#Chemokine
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Mikronischen der intratumoralen Mikrobiota beeinflussen die räumliche und zelluläre Heterogenität bei Krebs In einem kürzlich veröffentlichten Artikel in Naturkartierten die Forscher räumliche, zelluläre und molekulare Wechselwirkungen von Wirts- und tumorassoziierten Bakterien innerhalb der Tumormikroumgebung (TME). Sie verwendeten räumliche Profiling-Technologien in situ und Einzelzell-Ribonukleinsäuresequenzierung (scRNA-seq) und konzentrierten sich dabei auf Magen-Darm-Krebs, insbesondere orales Plattenepithelkarzinom (OSCC) und Darmkrebs (CRC). Lernen: Wirkung der intratumoral... #Bakterien #Bildgebung #CD4 #Chemokine #Darmkrebs #DNA_Schäden #DNS #Fisch #Fluoreszenz #Gen #Gensequenzierung #Hybridisierung #Immunität #in_vitro #Intrazellulär #Karzinom #Kinase #Kollagen #Kolorektal #Konfokale_Mikroskopie #Krebs #Makrophagen #Metastasierung #Mikroskopie #Monozyt #Neutrophile #Plattenepithelkarzinom #Präklinisch #Ribonukleinsäure #RNS #Transkription #Transkriptomie #tumor #Zelle
#DiseaseInfection_News#Medical_Research_News#Medical_Science_News#News#Bakterien#Bildgebung#CD4#Chemokine#Darmkrebs#DNA_Schäden#DNS#Fisch#Fluoreszenz#Gen#Gensequenzierung#Hybridisierung#Immunität#in_vitro#Intrazellulär#Karzinom#Kinase#Kollagen#Kolorektal#Konfokale_Mikroskopie#Krebs#Makrophagen#Metastasierung#Mikroskopie#Monozyt#Neutrophile
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Directing Traffic
Chemical messengers called chemokines are the traffic police of your body, telling cells on the move where to go via a chemokine concentration gradient. Atypical chemokine receptors (ACKRs) on certain cells help create these gradients by binding and engulfing specific chemokines. Three called GPR182, ACKR3 and ACKR4 are located in lymph and blood vessels, and research suggests may be found together in certain microenvironments within organs. However, there’s no comprehensive map of where they are. Researchers now genetically engineer mice with fluorescently-tagged GPR182, ACKR3, ACKR4 and ACKR-specific chemokines to locate them. Fluorescence microscopy revealed unique and shared distribution patterns of these ACKRs in a variety of organs, including the spleen (pictured, ACKR4 in green, GPR182 in red). Meanwhile, fluorescently-tagged chemokines revealed distinct activity zones for ACKR4 and GPR182 in the liver. These mouse models, therefore, provide a useful tool to probe ACKRs in different organs and microenvironments.
Written by Lux Fatimathas
Image from work by Serena Melgrati and colleagues
Institute for Research in Biomedicine, Università della Svizzera italiana, Bellinzona, Switzerland
Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)
Published in PLOS Biology, May 2023
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The human immune system is based on cells that communicate with each other via signaling molecules known as cytokines and chemokines. One of these signaling molecules is the protein MIF (macrophage migration inhibitory factor). It plays an important role in the regulation of various immune reactions by binding to suitable receptors of various cell types in a ternary complex, thereby activating certain signaling pathways in these cells. Surprisingly, there are plant proteins that are very similar to the human MIF protein in the sequence of their individual building blocks (amino acids) and these are referred to as MDL proteins. A team led by Jürgen Bernhagen from the Institute for Stroke and Dementia Research (ISD) at University of Munich Hospital and Professor Ralph Panstruga from the Unit of Plant Molecular Cell Biology at RWTH Aachen University in collaboration with a research group led by Professor Elias Lolis from Yale University in the U.S., has now shown that MIF and MDL proteins are also astonishingly similar in their spatial structure. Lead author Lukas Spiller and the team also found that the plant MDL proteins bind to the receptors of the MIF protein, alone or in complexes with the human MIF protein, and are thus able to activate immune-relevant signaling pathways—in some cases more efficiently than the human MIF protein alone.
Continue Reading.
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Reference archived on our website
Abstract
Objective COVID-19 induces the development of autoimmune diseases, including SLE, which are characterised by inflammation, autoantibodies and thrombosis. However, the effects of COVID-19 on SLE remain unclear.
Methods We investigated the effects of COVID-19 on SLE development and progression in three animal models. Plasmids encoding SARS-CoV-2 spike protein and ACE2 receptor were injected into R848-induced BALB/C lupus mice, R848-induced IL-1 receptor antagonist knockout (KO) lupus mice and MRL/lpr mice. Serum levels of albumin and autoantibodies, lymphocyte phenotypes and tissue histology were evaluated.
Results In R848-induced BALB/C lupus mice, the SARS-CoV-2 spike protein increased autoantibody and albumin levels compared with vehicle and mock treatments. These mice also exhibited splenomegaly, which was further exacerbated by the spike protein. Flow cytometric analysis revealed elevated T helper 1 cell counts, and histological analysis indicated increased levels of the fibrosis marker protein α-smooth muscle actin. In KO mice, the spike protein induced splenomegaly, severe kidney damage and pronounced lung fibrosis. In the MRL/lpr group, spike protein increased the serum levels of autoantibodies, albumin and the thrombosis marker chemokine (C-X-C motif) ligand 4.
Conclusion COVID-19 accelerated the development and progression of lupus by inducing autoantibody production, fibrosis and thrombosis.
#long covid#lupus#covid#covidー19#mask up#pandemic#covid 19#wear a mask#public health#coronavirus#sars cov 2#still coviding#wear a respirator#covid isn't over#covid conscious#covid is airborne#covid pandemic#covid19
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Human Cell Tournament Round 1
Propaganda!
ILC2 cells, or type 2 innate lymphoid cells are a type of innate lymphoid cell. Not to be confused with the ILC. They are derived from common lymphoid progenitor and belong to the lymphoid lineage. These cells lack antigen specific B or T cell receptor because of the lack of recombination activating gene. ILC2s produce type 2 cytokines (e.g. IL-4, IL-5, IL-9, IL-13) and are involved in responses to helminths, allergens, some viruses, such as influenza virus and cancer. ILC2s play the crucial role of secreting type 2 cytokines in response to large extracellular parasites. They express characteristic surface markers and receptors for chemokines, which are involved in distribution of lymphoid cells to specific organ sites. ILC2s are activated upon respiratory virus infections in mice and humans. For instance, during Influenza A virus infection, which induces IL-33 production, ILC2s are activated and drive airway hyper-responsiveness. [image credit]
The Y chromosome is one of two sex chromosomes in therian mammals and other organisms. Along with the X chromosome, it is part of the XY sex-determination system, in which the Y is the sex-determining chromosome because the presence of the Y chromosome causes offspring produced in sexual reproduction to be of male sex. In mammals, the Y chromosome contains the SRY gene, which triggers development of male gonads. The Y chromosome is passed only from male parents to male offspring. Most therian mammals have only one pair of sex chromosomes in each cell. Males have one Y chromosome and one X chromosome, while females have two X chromosomes. In mammals, the Y chromosome contains a gene, SRY, which triggers embryonic development as a male. The Y chromosomes of humans and other mammals also contain other genes needed for normal sperm production.
#lymphoid cells#y chromosome#poll#polls#tumblr poll#tumblr polls#tournament poll#wikipedia#cells of the human body#science tournament#biochemistry
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Note Cards (February 2024)
2nd Law and Acceleration
3' Untranslated Region
3rd Cuneiform Facet Shape
4th Rib and Age
18-Aldocorticosterone
30S Initiation Factors
Actions of Adductor Magnus
Age and Cranial Sutures
Ancylostoma duodenale Pathogenesis
Anthropological Linguistics
Brachialis OIA
Breeding Isolates
Causes of Negative Nitrogen Balance
Chemokines
Components of Hill Plots
Derivatives of Oxaloacetate
Echinococcosis
Endocrinology
Femoral Popliteal Surface
Fibularis Brevis
Flexor Digiti Minimi Brevis OIA
H. erectus at Ceprano Site
IgE
Ilex verticillata Names
Intermediate Filament
LCL vs MCL
Malate Dehydrogenase 1
Nail Matrix
Neanderthal Metabolism
Obturator Nerve Muscles
Parts of Epiphyses
Peptide Bond Structure
Primary vs Secondary Metabolites
sanguino-
Selective Pressures
Siding Metacarpal 3
Skull of Arago 21
Steps of Whole-Genome Shotgun Sequencing
Strongyloides stercoralis
Structure of α-Helix
T. Dale Stewart
T. trichiuria Appearance
Talus - Plantar View
Taphonomy
Teres Minor
Transcriptional Fusion
Trichuris trichiuria Pathogenesis
Vena Cava Inferior
venulo-
Zygomatic - Lateral View
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#studyblr#notes#studying#masterlist#study masterlist#master list#study master list#studyblr resources#study resources#learning#learning resources#school#school resources#free learning#science#academics#academia#learning science#mcat resources#mcat notes#mcat studyblr#mcat masterlist#resource masterlist#scienceblr#medblr
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Wren your egg lore is so interesting
Thank you!! Without spoiling too much, I'll tell you a bit about how it is the 'egg' spores infect their host, scientifically speaking. (from discord) Basically, premature spores get inside an open wound and into the bloodstream. From there they release proteins that are similar in structure to a certain immune cell, allowing them to stay undetected by the immune system. These spores also have immunosupressing effects. The spores make their way into the central nervous system via the bloodstream. SEM spores in addition to already being similar in shape and structure to helper T-cells, which are critical to the process of activating the immune system against threats. The spores are disguised as Helper T-cells, and even produce their own chemical signals altering other immune cells. From there, they circulate throughout the body undetected by other immune cells due to the proteins and chemical signals the spores produce. Once into the bloodstream, the disguised spores make their way into the right and left common carotid arteries, which are located in the neck. As the spores travel deeper into the internal carotid arteries, these disguised cells end up at the cerebral capillary wall and penetrate it through extravasation. This includes producing a special Exoenzyme signal to essentially trick the endothelial cells into opening up- and allowing the spores into the brain tissue. From there, they use chemokines to navigate to the cerebral cortex.
#thanks for the ask!#the wren calls#mcyt#mcytblr#mcyt worldbuilding#dream smp#dsmp#dsmpblr#dsmp lore#tw medical#tw fungi#egg arc#egg lore#eggpire#speculative biology#speculative immunology#the fungus among us chronicles
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Pneumonia In Children And Adults
Introduction
Pneumonia stands as a prevalent respiratory infection, exerting a significant burden on global public health. Its impact extends beyond mere morbidity, contributing to substantial healthcare costs and socioeconomic consequences. This discussion aims to elucidate the general nature of pneumonia, encompassing its pathophysiology, clinical presentation, diagnostic modalities, treatment strategies, complications, and preventive measures. By indulging into these factors, we aim to provide a better understanding of pneumonia’s complexity and underscore the importance of timely recognition and management.
Pathophysiology
Pneumonia ensues from the infiltration of infectious agents, including bacteria, viruses, fungi, and less commonly, parasites, into the lower respiratory tract. Upon inhalation or aspiration of these pathogens, they gain access to the alveoli, where they incite an inflammatory response. This inflammatory cascade triggers the release of pro-inflammatory cytokines and chemokines, recruiting immune cells to the site of infection. Neutrophils, macrophages, and lymphocytes converge to eradicate the invading pathogens, leading to the characteristic consolidation and exudate formation within the affected lung tissue. As the infection progresses, alveolar edema, impaired gas exchange, and parenchymal damage ensue, culminating in the clinical manifestations of pneumonia.
Clinical Presentation
The clinical presentation of pneumonia encompasses a spectrum of symptoms, ranging from mild respiratory complaints to life-threatening respiratory failure. Common symptoms include cough, productive sputum production, fever, chills, pleuritic chest pain, dyspnea, tachypnea, and systemic manifestations such as malaise and fatigue. The severity of symptoms varies depending on factors such as the underlying pathogen, the extent of lung involvement, the host’s immune status, and comorbidities. In pediatric populations, pneumonia may present with nonspecific symptoms such as feeding difficulties, lethargy, and irritability, posing diagnostic challenges. Conversely, elderly individuals may exhibit atypical presentations characterized by confusion, hypothermia, and exacerbations of underlying chronic conditions.
Diagnostic Modalities
The diagnosis of pneumonia hinges on a comprehensive clinical assessment, augmented by various diagnostic modalities to confirm the presence of pulmonary infection and reveal its etiology. A thorough history and physical examination provide invaluable insights into the patient’s symptomatology, risk factors, and clinical trajectory. Symptomatic findings such as crackles, wheezes, and diminished breath sounds may aid in localizing the site of infection and assessing disease severity. Radiographic imaging, notably chest X-rays and computed tomography (CT) scans, serves as the cornerstone of pneumonia diagnosis, revealing characteristic radiographic findings such as airspace opacities, lobar consolidation, and interstitial infiltrates. Laboratory investigations, including complete blood count (CBC), C-reactive protein (CRP), and procalcitonin levels, may corroborate the clinical suspicion of pneumonia and guide therapeutic decisions. Additionally, microbiological testing of respiratory specimens through techniques such as sputum culture, blood cultures, and polymerase chain reaction (PCR) assays facilitates pathogen identification and antimicrobial susceptibility testing, thereby informing targeted therapy.
Treatment Strategies
The management of pneumonia hinges on prompt initiation of empiric antimicrobial therapy tailored to the likely causative pathogen(s) and disease severity. Antibiotics represent the mainstay of treatment for bacterial pneumonia, with the choice of agent dictated by factors such as local antimicrobial resistance patterns, patient age, comorbidities, and recent antibiotic exposure. Commonly prescribed antibiotics include beta-lactam agents (e.g., penicillins, cephalosporins), macrolides, fluoroquinolones, and combination regimens for severe or healthcare-associated infections. Conversely, viral pneumonia necessitates supportive care measures, given the limited efficacy of antiviral agents in most cases. Influenza-associated pneumonia may benefit from neuraminidase inhibitors such as oseltamivir, while respiratory syncytial virus (RSV) pneumonia may warrant ribavirin therapy in select cases. Adjunctive therapies such as oxygen supplementation, bronchodilators, and corticosteroids may mitigate respiratory distress and improve clinical outcomes, particularly in severe or hypoxemic patients. The duration of antimicrobial therapy varies depending on factors such as the causative pathogen, clinical response, radiographic resolution, and the presence of complications. Close monitoring of clinical parameters and serial imaging studies guide the decision-making process, enabling clinicians to tailor therapy to individual patient needs.
Complications
Pneumonia harbors the potential for various complications, ranging from mild to life-threatening sequelae, necessitating vigilant monitoring and timely intervention. Common complications include pleural effusion, empyema, lung abscess, respiratory failure, septic shock, and acute respiratory distress syndrome (ARDS). Pleural effusion denotes the accumulation of fluid within the pleural space, secondary to inflammation or impaired lymphatic drainage, manifesting as dyspnea, pleuritic chest pain, and dullness to percussion on physical examination. Empyema represents a purulent collection within the pleural cavity, often complicating bacterial pneumonia and necessitating drainage via thoracentesis or chest tube placement. Lung abscesses manifest as circumscribed cavities containing necrotic debris and pus within the lung parenchyma, triggered by persistent fever, productive cough, and hemoptysis. Respiratory failure ensues from impaired gas exchange and alveolar hypoventilation, caused by worsening hypoxemia, hypercapnia, and respiratory acidosis, necessitating mechanical ventilation and intensive care support. Septic shock represents a life-threatening complication of severe pneumonia, characterized by systemic inflammatory response syndrome (SIRS) and end-organ dysfunction, requiring aggressive fluid resuscitation, vasopressor therapy, and broad-spectrum antibiotics. ARDS denotes a severe form of acute lung injury, characterized by diffuse alveolar damage, refractory hypoxemia, and bilateral infiltrates on chest imaging, necessitating lung-protective ventilation and supportive care in the intensive care unit (ICU). The occurrence of complications portends a poor prognosis and underscores the need for early recognition and intervention to mitigate adverse outcomes.
Preventive Measures
Preventing pneumonia entails a broad approach encompassing vaccination, infection control measures, and health promotion strategies aimed at reducing the risk of respiratory infections and their sequelae. Vaccination stands as a cornerstone of pneumonia prevention, targeting common bacterial and viral pathogens implicated in pneumonia pathogenesis. Vaccines such as the pneumococcal conjugate vaccine (PCV13) and pneumococcal polysaccharide vaccine (PPSV23) confer protection against Streptococcus pneumoniae, the leading bacterial cause of pneumonia, particularly in high-risk populations such as young children, older adults, and immunocompromised individuals. Influenza vaccination remains paramount in mitigating influenza-associated pneumonia and reducing disease transmission, underscoring the importance of annual vaccination campaigns targeting vulnerable populations. Additionally, adherence to infection control measures, including hand hygiene, respiratory etiquette, and environmental sanitation, plays a pivotal role in reducing the spread of respiratory pathogens in healthcare settings and the community at large. Health promotion efforts aimed at smoking cessation, optimizing nutrition, and addressing underlying comorbidities such as chronic obstructive pulmonary disease (COPD), asthma, and immunodeficiency bolster immune resilience and mitigate pneumonia risk. Furthermore, early identification and management of predisposing factors such as malnutrition, homelessness, and overcrowded living conditions attenuate pneumonia susceptibility and enhance overall health outcomes.
Conclusion
In conclusion, pneumonia emerges as a formidable respiratory infection, posing significant challenges to global public health. Its diverse etiology, clinical manifestations, diagnostic modalities, treatment modalities, complications, and preventive measures underscore the nature of pneumonia management. Timely recognition and intervention are imperative in mitigating the morbidity and mortality associated with pneumonia, necessitating a collaborative approach among healthcare providers, public health authorities, and policymakers. By fostering a comprehensive understanding of pneumonia’s manifest and implementing evidence-based strategies, we can strive towards reducing its burden and improving patient outcomes. Through ongoing research, education, and advocacy efforts, we can envision a future where pneumonia-related morbidity and mortality are substantially diminished, paving the way for enhanced respiratory health and well-being worldwide.
In managing pneumonia, compassion, empathy, and a holistic approach are essential alongside clinical expertise. Striving for excellence in knowledge and practice allows us to enhance respiratory medicine and patient outcomes.
As we address pneumonia and broader cardiovascular health complexities, let’s remain committed to optimal patient care. Together, we can impact lives positively and foster a healthier future.
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Does Inflammation Help Healing
The immune system's normal reaction to damage, infection, or foreign substances is inflammation. It's a complex process that includes the creation of inflammatory mediators like chemokines and cytokines in addition to the activation of various immune cells. Despite the fact that inflammation is frequently associated with discomfort, swelling, and redness, it is a crucial step in the healing process.
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Neuartiger Radiotracer für molekulare Bildgebung kann mehrere Krebsarten präzise diagnostizieren Ein neuer Radiotracer für molekulare Bildgebung kann eine Vielzahl von Krebsarten präzise diagnostizieren und bietet einen Fahrplan zur Identifizierung von Patienten, die von gezielten Radionuklidtherapien profitieren könnten. In der größten medizinischen Studie dieser Art fanden die Forscher heraus, dass 68Ga-PentixaFor einen hohen Bildkontrast bei hämatologischen Malignomen, kleinzelligem Lungenkrebs und Nebennierenrindentumoren zeigte. Diese Forschung wurde in der Novembera... #Adenom #Bildgebung #Chemokin #CT #Diabetes #Endokrinologie #Forschung #Gastroenterologie #Hämatologie #Karzinom #Kleinzelliger_Lungenkrebs #Krankenhaus #Krebs #Lungenkrebs #Lymphom #Maligne #Mantelzell_Lymphom #Medizin #Molekulare_Bildgebung #Multiples_Myelom #Myelom #Nebennierenrindenkarzinom #Nuklearmedizin #Onkologie #Präzisionsmedizin #Radiologie #Radionuklid #Rezeptor #Theranostik #tumor #Zahnheilkunde #Zelle
#Medical_Condition_News#Medical_Research_News#Medical_Science_News#News#Adenom#Bildgebung#Chemokin#CT#Diabetes#Endokrinologie#Forschung#Gastroenterologie#Hämatologie#Karzinom#Kleinzelliger_Lungenkrebs#Krankenhaus#Krebs#Lungenkrebs#Lymphom#Maligne#Mantelzell_Lymphom#Medizin#Molekulare_Bildgebung#Multiples_Myelom#Myelom#Nebennierenrindenkarzinom#Nuklearmedizin#Onkologie#Präzisionsmedizin#Radiologie
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Cytokines and their role in health and disease
The aetiology of human diseases is complicated, as is our immune system. The human body relies on a process known as the cell signalling system to prevent diseases. This pathway involves a series of chemical events between a cluster of molecules within a cell that control the activity of a cell, such as cell division or cell death.
When a substance, such as a hormone or growth factor, binds to a specific protein receptor on or in the cell, the cell receives signals from its surroundings. The first molecule in the pathway receives a signal, activating a subsequent molecule. This process is continued throughout the signalling pathway until the final molecule is activated and the cell function is completed.
Immune response is mediated by cellular signalling. Defects and irregularities in cellular pathways are frequently the core cause of many diseases such as cancer, respiratory and autoimmune disorders.
Studies show that cytokines play a crucial role in cellular signalling. Cells release tiny proteins that influence the behaviour of other cells. Cytokines, which work as cell messengers, are in charge of controlling the formation and function of other blood and immune system cells.
In this article, we demystify the role of cytokines by explaining how they work, their types, their functions, and their importance in health and disease.
What are cytokines?
Medically speaking, cytokines are multifunctional polypeptide hormones or small proteins, non-structured and light in terms of molecular weight, that are released by several types of cells. These proteins influence and regulate a range of biological processes such as immunity and inflammation. Cytokine proteins are soluble and are vital to our immune system. Cytokine portfolio is crucial to the functions of macrophages that act as guards to the innate immune system and bring about the conversion from innate to adaptive immunity.
In other words, they act as messengers and mediate complex synergies between immune and non-immune cells, such as:
· hematopoietic cells,
· lymphoid cell, and
· various pro-inflammatory and anti-inflammatory cells that stimulate the growth of inflammatory and immune responses.
Cytokine activity was recognised and established between the years 1940- 1960. There are about 200 cytokines that have been recognized to date.
Based on their properties, their secretion, and effect on the immune response, cytokines can be broadly divided into the following categories:
Proinflammatory cytokines: These cytokines are associated with inflammatory responses (amplification and perpetuation of the inflammatory process).
Growth factors: These cytokines promote cell survival and bring about structural changes in the airways.
Anti-inflammatory: Anti-inflammatory cytokines control the pro-inflammatory cytokine reaction.
What are the different types of cytokines?
Since Cytokines have several diverse biological functions, there are many different types of Cytokines. Cytokines being a broad term, some of the more specific proteins that fall under this family based on their functions include:
· chemokines (CC, CXC, CX3C, and XC),
· interferons (IFN)
· interleukins (IL),
· lymphokines,
· tumour necrosis factor (TNF) and
· growth factors.
Chemokines play a vital role in the migration of leukocyte cells and are related to chemotactic effects for inflammatory cells.
Interferons aid the body’s defence against cancer and viral diseases.
Lymphokines are produced by lymphocytes. These cytokines attract immune cells such as macrophages. These cytokines are secreted by T cells (that grow from stem cells in the bone marrow) and control the immune response.
Interleukins are a group of cytokines that act as chemical signals between white blood cells and are produced by a single leukocyte. They can act on other leukocytes, mediating interactions among cells. Specific interleukins can have a significant impact on cell-cell communication.
Tumour necrosis factor or TNF cytokines are released in case an infection is detected by macrophages (specific white blood cells) to signal other cells of the immune system to trigger an inflammatory response.
When discussing cytokines as growth factors, it is necessary to note growth factors signal a positive effect on cell division, whereas cytokine is a term that is neutral for whether a molecule has an impact on reproduction. While some cytokines can operate as growth factors, others can impede cell growth. Some trigger programmed cell death in target cells by acting as “death” signals. For instance, cytokines promote anti-cancer activity and help prevent disease by releasing signals that can cause abnormal cells to die and normal cells to live longer.
What are the functions of cytokines?
Cytokine proteins act through receptors found on the membranes of responsive target cells and are essential in the immune system.
They
· modulate the balance between humoral and cell-based immune responses,
· induce inflammatory response,
· regulate hematopoiesis,
· differentiate and induce wound healing, and
· regulate certain cell populations’ maturation, growth, and responsiveness.
In addition, cytokines frequently trigger the production of new cytokines, causing a cascade of events in which the latter cytokines affect the activity of the previous cytokines that released them.
Lastly, due to their brief half-lives in the blood and extracellular fluids, they have a short functional range.
How are Cytokines produced?
Cytokines are mainly produced by a broad range of cells, including immune cells like:
· macrophages,
· B lymphocytes,
· T lymphocytes and
· mast cells.
These proteins can also be produced by endothelial cells, polymorphonuclear leukocytes (PMN), epithelial cells, connective tissue, and adipocytes.
What is the importance of cytokines in health and disease?
They are essential in health and disease, specifically in host responses to infection, immune cell differentiation and responses, trauma, inflammation, sepsis, reproduction, viral pathogenesis, neurobiology, angiogenesis, tumorigenesis, etc. Apart from innate and adaptive immunity, cytokines are now also significant in the fields of cancer and atherosclerosis.
Cytokines can therefore contribute in therapy and as prognostic and diagnostic agents while also being effective biomarkers for health and disease. Cytokines in therapy such as IL-1 and IL-2 are likely to act as natural immuno-stimulants to fight against the immune deficiency of AIDS. This hypothesis is supported by experimental and clinical studies which state that immune-stimulant cytokines have a potential to aid in the neutralisation of the immune-suppression of cancer and AIDS.
Specific cytokines used in treating cancer can be produced in a lab. Some cytokines are effective in reducing or controlling the side effects of chemotherapy. Interleukins and interferons are the most used.
Helvetica Health Care (HHC) specialises in the production and supply of CELLKINES™ product line that consists of Human Interleukin-2 (IL-2), also referred to as T-CELL GROWTH FACTOR (TCGF). Natural Human IL-2 remains the preferred choice for lymphocyte cell stimulation in culture. Additionally, Recombinant IL-2 produced in E. coli is also available.
At HHC, we strive to supply innovative life science products and technologies of the highest quality to manage health and improve the quality of life. Thanks to our successful partnerships with our collaborators, we guarantee timely and risk-free deliveries with optimal care within 48 hours from our warehouse in Geneva.
Contact HHC today and find out how we can help you!
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Roles of the SARS-CoV-2 spike protein during infection and inflammation.
(A) The spike protein (red) binds to the angiotensin-converting enzyme 2 (ACE2, orange) on the surface of epithelial cells, leading to the virus entering the cells.
(B) Khan et al. artificially introduced a plasmid containing the DNA sequence for the spike protein to epithelial cells (bottom) which were cultured together with macrophages (top) in the laboratory. This caused the epithelial cells to make the spike protein, which triggered the macrophages to produce pro-inflammatory cytokines and chemokines. However, under these conditions, the spike protein was not detected in the culture medium, suggesting that the macrophages are somehow able to sense the protein either inside or on the surface of epithelial cells. This activation requires the spike protein to bind to Toll-like receptors (TLRs) that have formed dimers – either TLR2 with TLR1, or TLR2 with TLR6. Adaptor protein MyD88 then activates a transcription factor, nuclear factor-κB (NF-κB), which induces the transcription of pro-inflammatory molecules.
(C) Khan et al. also used a plasmid to produce recombinant spike protein in the laboratory, and then applied these proteins to the medium in which macrophages and epithelial cells were growing. This showed that the spike protein can trigger both types of cells to produce pro-inflammatory cytokines and chemokines. This activation also required the TLR dimers and MyD88.
#inflammation#cardiovascular disease#covid-19 vaccine#covid-19#spike protein#fav#print this off later
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SARS-CoV-2 Selectively Induces the Expression of Unproductive Splicing Isoforms of Interferon, Class I MHC, and Splicing Machinery Genes - Published May 23, 2024
Abstract RNA processing is a highly conserved mechanism that serves as a pivotal regulator of gene expression. Alternative processing generates transcripts that can still be translated but lead to potentially nonfunctional proteins. A plethora of respiratory viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), strategically manipulate the host’s RNA processing machinery to circumvent antiviral responses. We integrated publicly available omics datasets to systematically analyze isoform-level expression and delineate the nascent peptide landscape of SARS-CoV-2-infected human cells. Our findings explore a suggested but uncharacterized mechanism, whereby SARS-CoV-2 infection induces the predominant expression of unproductive splicing isoforms in key IFN signaling, interferon-stimulated (ISGs), class I MHC, and splicing machinery genes, including IRF7, HLA-B, and HNRNPH1. In stark contrast, cytokine and chemokine genes, such as IL6 and TNF, predominantly express productive (protein-coding) splicing isoforms in response to SARS-CoV-2 infection. We postulate that SARS-CoV-2 employs an unreported tactic of exploiting the host splicing machinery to bolster viral replication and subvert the immune response by selectively upregulating unproductive splicing isoforms from antigen presentation and antiviral response genes. Our study sheds new light on the molecular interplay between SARS-CoV-2 and the host immune system, offering a foundation for the development of novel therapeutic strategies to combat COVID-19.
#covid#mask up#pandemic#covid 19#wear a mask#coronavirus#sars cov 2#still coviding#wear a respirator#public health#long covid
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Global C-X-C Chemokine Receptor 4 (CXCR4) Antagonists Market Analysis 2024: Size Forecast and Growth Prospects
The c-x-c chemokine receptor 4 (cxcr4) antagonists global market report 2024 from The Business Research Company provides comprehensive market statistics, including global market size, regional shares, competitor market share, detailed segments, trends, and opportunities. This report offers an in-depth analysis of current and future industry scenarios, delivering a complete perspective for thriving in the industrial automation software market.
C-X-C Chemokine Receptor 4 (CXCR4) Antagonists Market, 2024 report by The Business Research Company offers comprehensive insights into the current state of the market and highlights future growth opportunities.
Market Size - The C-X-C chemokine receptor 4 (CXCR4) antagonist market size has grown strongly in recent years. It will grow from $1.49 billion in 2023 to $1.62 billion in 2024 at a compound annual growth rate (CAGR) of 9.3%. The growth in the historic period can be attributed to increasing transparency in clinical trial data, patient-centric healthcare policies, rising prevalence of chemotherapy resistance, policies emphasizing patient-centered care and access, and increasing preference for targeted therapies.
The C-X-C chemokine receptor 4 (CXCR4) antagonist market size is expected to see strong growth in the next few years. It will grow to $2.33 billion in 2028 at a compound annual growth rate (CAGR) of 9.4%. The growth in the forecast period can be attributed to expanding applications in HIV or AIDS, rising demand for stem cell mobilization, potential in autoimmune diseases, growth in biobanking initiatives, and integration of artificial intelligence (AI) in drug discovery. Major trends in the forecast period include increasing focus on orphan drug development, development of combination therapies, adoption of precision oncology approaches, expanding clinical trials for novel therapies, and advancements in drug delivery technologies.
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Scope Of C-X-C Chemokine Receptor 4 (CXCR4) Antagonists Market The Business Research Company's reports encompass a wide range of information, including:
1. Market Size (Historic and Forecast): Analysis of the market's historical performance and projections for future growth.
2. Drivers: Examination of the key factors propelling market growth.
3. Trends: Identification of emerging trends and patterns shaping the market landscape.
4. Key Segments: Breakdown of the market into its primary segments and their respective performance.
5. Focus Regions and Geographies: Insight into the most critical regions and geographical areas influencing the market.
6. Macro Economic Factors: Assessment of broader economic elements impacting the market.
C-X-C Chemokine Receptor 4 (CXCR4) Antagonists Market Overview
Market Drivers - The increase in the prevalence of human immunodeficiency virus (HIV) is expected to propel the growth of the spasmodic dysphonia treatment market going forward. Human immunodeficiency virus (HIV) is a virus that targets and weakens the immune system by attacking CD4 (T) cells, potentially leading to AIDS if left untreated. HIV prevalence is rising due to low awareness, limited healthcare access, higher transmission rates, and inadequate prevention in some areas. CXCR4 antagonists block the CXCR4 receptor, stopping HIV from accessing and infecting immune cells, which aids in controlling the virus and enhancing the immune response. For instance, according to Joint United Nations Programme on HIV/AIDS (UNAIDS), in 2022, there were 39 million [33.1 million-45.7 million] HIV-positive people worldwide, with 1.3 million [1 million-1.7 million] people newly infected with HIV in 2022. Therefore, the increase in the prevalence of human immunodeficiency virus (HIV) is driving the growth of the CXCR4 antagonist market.
Market Trends - Major companies operating in the CXCR4 antagonist market are focusing on developing bioequivalents to enhance treatment options and improve patient outcomes in various diseases. Bioequivalent refers to pharmaceutical products with similar bioavailability when compared under similar conditions. For instance, in May 2024, Gland Pharma, an India-based generic injectable manufacturing company, received approval from the United States Food and Drug Administration (US FDA) for Plerixafor Injection. The approved product is bioequivalent and therapeutically equivalent to the reference listed drug (RLD), MOZOBIL (plerixafor) injection of Genzyme Corporation. Plerixafor is a CXCR4 antagonist that, when used with granulocyte-colony stimulating factor, helps to mobilize hematopoietic stem cells into the peripheral blood for collection and autologous transplantation in patients with non-Hodgkin's lymphoma and multiple myeloma.
The C-X-C chemokine receptor 4 (CXCR4) antagonists market covered in this report is segmented –
1) By Type: BL-8040, GMI-1359, Plerixafor (AMD3100), Balixafortide (POL6326), USL311, Burixafor (GPC-100), Other Types 2) By Route Of Administration: Oral, Injectable 3) By Product Pipeline: Approved, Clinical Trials, Pre-Clinical 4) By Application: Cancer, Human Immunodeficiency Virus (HIV), Chronic Inflammatory Disease, Stem Cell Mobilization, Immune And Autoimmune Diseases 5) By Distribution Channel: Hospital Pharmacies, Retail Pharmacies, Online Pharmacies
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Regional Insights - North America was the largest region in the C-X-C chemokine receptor type 4 antagonists market in 2023. The regions covered in the C-X-C chemokine receptor 4 (CXCR4) antagonists market report are Asia-Pacific, Western Europe, Eastern Europe, North America, South America, Middle East, Africa.
Key Companies - Major companies operating in the C-X-C chemokine receptor 4 (CXCR4) antagonists market are Pfizer Inc., F-Hoffmann La Roche Ltd., Sanofi, Bristol-Myers Squibb Company, AstraZeneca plc, GlaxoSmithKline, Eli Lilly and Company, Amgen Inc., Takeda Chemical Industries Ltd., Kyowa Kirin Co. Ltd., BioLegend Inc., Kura Oncology Inc., CUSABIO TECHNOLOGY LLC, Cayman Chemical, X4 Pharmaceuticals Inc., BioLineRx Ltd., Spexis Ltd., Biokine Therapeutics Ltd., GlycoMimetics, AnorMED Inc., CohBar Inc.
Table of Contents 1. Executive Summary 2. C-X-C Chemokine Receptor 4 (CXCR4) Antagonists Market Report Structure 3. C-X-C Chemokine Receptor 4 (CXCR4) Antagonists Market Trends And Strategies 4. C-X-C Chemokine Receptor 4 (CXCR4) Antagonists Market – Macro Economic Scenario 5. C-X-C Chemokine Receptor 4 (CXCR4) Antagonists Market Size And Growth ….. 27. C-X-C Chemokine Receptor 4 (CXCR4) Antagonists Market Competitor Landscape And Company Profiles 28. Key Mergers And Acquisitions 29. Future Outlook and Potential Analysis 30. Appendix
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Quantitative proteomics reveals differential extracellular vesicle cargo from M1 and M2 monocyte-derived human macrophages
Extracellular vesicles (EVs) mediate intercellular communication by carrying molecular cargo that 2 facilitate diverse physiological processes. Macrophages, playing central roles in immune responses, 3 release EVs that modulate various cellular functions. Given the distinct roles of M1 and M2 4 macrophage states, understanding the proteomic profiles of their EVs is important for elucidation of 5 EV-mediated signalling and identifying potential biomarkers for diseases involving macrophage 6 polarisation. We employed quantitative proteomics combined with bioinformatics to characterise 7 the proteomic profile of EVs released by M1 and M2 monocyte-derived macrophages. We identified 8 1,731 proteins in M1/M2 EVs, 132 of which were significantly differentially between M1 and M2. 9 Proteomic data, together with pathway analysis, found that M1/M2 macrophage EV cargo relate to 10 cellular source, and may play roles in shaping immune responses, with M1 EV cargo associated with 11 promotion of pro-inflammatory and antiviral functions, while M2 EV cargo associated with immune 12 regulation and tissue repair. M1 EV cargo was associated with cytokine/chemokine signalling 13 pathways, DNA damage, methylation, and oxidative stress. M2 EV cargo were associated with 14 macrophage alternative-activation signalling pathways, antigen presentation, and lipid metabolism. 15 We also report that macrophage EVs carry metallothioneins, and other related proteins involved in 16 response to metals and oxidative stress. http://dlvr.it/TDXNKy
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