#interleukin-6

[medicomunicare]

Depression "under pressure": the better we know mechanisms, the better come out managements

Deporession ad public health emergency Depression is a growing mental health concern and is associated with significant levels of disability across the world. Depressive symptoms, such as persistent low mood, fatigue, cognitive impairments, anhedonia, or a lack of interest or pleasure in the activities of life, are categorized as interest-activity symptoms. These symptoms contribute substantially…

[jppres]

The role of plasma angiotensin-converting enzyme and interleukin-6 levels on the prognosis of non-dialysis chronic kidney disease patients

Image: Max Pixel Article published in J. Pharm. Pharmacogn. Res., vol. 11, no. 1, pp. 55-62, January-February 2023. DOI: https://doi.org/10.56499/jppres22.1518_11.1.55 Hendri Susilo1,2**, Mochammad Thaha3,4, Budi Susetyo Pikir1,2, Mochamad Yusuf Alsagaff1,2, Satriyo Dwi Suryantoro3,4, Ifan Ali Wafa5, Nando Reza Pratama5, David Setyo Budi5, Bayu Satria Wiratama6, Citrawati Dyah Kencono…

[bpod-bpod]

Culture of Disorder

Human neural progenitor cells generated from induced pluripotent stem cells – cells from reprogrammed mature cells – for modelling effects of pro-inflammatory molecule IL-6 released in maternal immune activation, a potential contributor to neurodevelopmental disorders in the offspring

Read the published research paper here

Image from work by Kseniia Sarieva and colleagues

Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in and cover image of Disease Models & Mechanisms, November 2023

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[mitalipingale]

https://bundas24.com/read-blog/112096_interleukin-6-il-6-inhibitors-market-size-analysis-and-forecast-2031.html

The Interleukin-6 (IL-6) Inhibitors Market in 2023 is US$ 33.3 billion, and is expected to reach US$ 77.41 billion by 2031 at a CAGR of 11.12%.

[tchaikovskym]

data analysis is so draining but man i have correlations!!

[covid-safer-hotties]

Also preserved in our archive

"Just a cold" that increases intercranial abnormalities

By Nikhil Prasad

Medical News: A groundbreaking study conducted at San Marco University Hospital in Catania, Sicily, Italy, has revealed new insights into the potential impacts of SARS-CoV-2 on newborns. Researchers from this hospital and the University of Ferrara carried out an ultrasonographic analysis on newborns exposed to the virus, highlighting a significant incidence of minor intracranial abnormalities compared to unexposed infants. The findings raise important questions about the long-term neurological implications for children born during the COVID-19 pandemic.

The Study at a Glance This Medical News report delves into the research conducted by Bruna Scalia, Marco Andrea Nicola Saporito, and their colleagues, investigating cranial ultrasonography (cUS) findings in infants born to mothers who tested positive for SARS-CoV-2 during pregnancy or at delivery. The team analyzed data from 278 newborns, evenly split between exposed and unexposed cohorts. The study adhered to stringent observational protocols to ensure the reliability of results.

Key Findings Among the 139 newborns exposed to SARS-CoV-2, 23% exhibited intracranial abnormalities on cUS, compared to 16.5% in the unexposed group. Minor abnormalities were most prevalent and included subependymal cysts (SEPCs), choroid plexus cysts (CPCs), frontal horn cysts (FHCs), and lenticulostriate vasculopathy (LV). Major abnormalities, such as cerebellar hemorrhages and arachnoid cysts, were rare but noteworthy.

Interestingly, infants exposed to SARS-CoV-2 during pregnancy had a higher rate of abnormalities (38.4%) than those exposed at birth (19.5%). The second trimester emerged as a particularly critical period, with the majority of abnormalities observed in this subgroup.

Why These Findings Matter The study's results are alarming for public health professionals and expectant mothers. While SARS-CoV-2's immediate risks to newborns have been considered minimal, this research suggests subtle yet significant neurological effects. These abnormalities, although classified as minor, may carry long-term implications for cognitive and behavioral development.

The link between maternal inflammation and fetal development is not new, but the cytokine storm induced by SARS-CoV-2 appears to heighten this risk. The researchers hypothesize that inflammatory markers like interleukin-6 could cross the placenta, affecting the fetal brain and potentially disrupting synaptogenesis.

Methodology Details All newborns in the study underwent cranial ultrasonography within their first week of life. The scans were conducted using standardized equipment by experienced neonatologists. The findings were categorized as normal, minor, or major abnormalities. To exclude confounding factors, the study excluded infants with other infections or genetic disorders.

Demographic factors, such as gestational age and birth weight, were comparable across both groups. However, premature birth and maternal complications, such as gestational diabetes and hypertension, were noted as potential contributors to the observed abnormalities.

Implications for Future Research The findings call for more extensive, longitudinal studies to understand the long-term effects of these abnormalities. Current evidence suggests a potential association between minor abnormalities like SEPCs and neuropsychiatric conditions such as autism and ADHD. Further investigation could clarify whether these cUS findings are precursors to such outcomes.

What Experts Are Saying The study's authors emphasize caution, noting that minor intracranial abnormalities do not necessarily predict adverse outcomes. However, they recommend routine cranial ultrasonography for newborns exposed to SARS-CoV-2 as a precautionary measure. "The cost-effectiveness and non-invasive nature of cUS make it a valuable tool in monitoring these infants," said lead researcher Bruna Scalia.

Limitations and Strengths of the Study One limitation of the study was its relatively small sample size, particularly for subgroups like prenatally exposed infants. Additionally, the lack of serological testing for unexposed mothers could have introduced undetected cases into the control group. However, the study's rigorous methodology and use of a well-matched control group lend credibility to its conclusions.

Study Conclusions The research underscores a statistically significant increase in minor intracranial abnormalities among SARS-CoV-2-exposed newborns. These findings are particularly pronounced in infants exposed during the second trimester of pregnancy. While the abnormalities observed in the study were predominantly minor, their potential impact on long-term neurological outcomes cannot be overlooked. The researchers advocate for the following:

-Routine cUS Screening: Cranial ultrasonography should be performed on all newborns exposed to SARS-CoV-2 to identify abnormalities early.

-Long-Term Follow-Up: Exposed infants should be enrolled in neurodevelopmental follow-up programs to monitor their progress and intervene if necessary.

-Expanded Research: Larger, multicenter studies are needed to confirm these findings and explore the mechanisms behind SARS-CoV-2's impact on fetal brain development.

By highlighting these abnormalities, the study adds a critical layer to our understanding of COVID-19's broader implications, particularly for future generations.

The study findings were published in the peer-reviewed Italian Journal of Pediatrics. link.springer.com/article/10.1186/s13052-024-01826-3

[mleprae]

Cytokines are so cute, you know those weird numbers you see in medical text? The one you'll likely see around is Interleukin, shortned to IL. The name literally means 'Cell communication', they're chemicals that cells release to speak to one another, depending what interleukin you find in a test, you can deduce what these little guys are planning and doing at the moment

The most common ones are TNF-a (tumor necrosis alpha) and IL-6, both stimulate inflammation in damaged area. Inflammation is just the cells setting up the battlefield, the redness is due to bloodflow in the area bringing more immune cells in, the pain is that sometimes the area increases, pressing onto nerves. It's your body telling you that you need to stop using that part.

IL-6 and TNF-a are the cytokines that the cells use to call one another, kind of a "I need backup here" signal. Some of these cytokines are pyrogenic, which is what we call the ones that go to the brain and tell it to raise body temperature!

You also have interferons (shortned to IFN), those are what cells produce to warn others in a "I'm infected with something, stay away" kind of way, this tells the other cells that they need to protect themselves, it also calls some cells responsible to kill infected cells to do their jobs

[auszeitstille]

Millions missing

Knapp 1 1/2 Jahre sind vergangen, seit dem ersten Verdacht, an ME/CFS erkrankt zu sein. Und dem langsamen Verschwinden, aus meinem eigenen Leben.

Kurze Zeit später fand ich raus, dass überdurchschnittlich viele, eine positive EBV Anamnese haben. Ein Virus, das meiner Meinung nach jahrzehntelang unterschätzt wurde. Dabei setzt diese Erkrankung so viele von uns, völlig außer Gefecht und befördert einige ins Krankenhaus, wie auch mich, damals mit 13 Jahren.

Angegriffene Organe, der gesamte Organismus völlig aus dem Gleichgewicht. Lebenslanges Risiko der Reaktivierung, Chronifizierung und mögliche Ursache, einer am Ende unheilbaren Erkrankung. Aber wer hätte das schon ahnen können? Am allerwenigsten ich selbst.

8 Monate, seit ich geschwächt bei meiner Hausärztin saß und ihr berichtete, dass ich nach einem schweren, aber unklaren Infekt im Sommer 2020, nicht wieder auf die Beine kam; dass ich mich mittlerweile seit Monaten krank fühle. Tägliche Grippesymptome, neurologische und motorische Ausfälle, eine bleierne Erschöpfung und starke Schmerzen.

Sie hat mich nicht ernst genommen. Der Klassiker. Schließlich war ich untergewichtig und steckte wieder tief in der Essstörung.

Für sie war mein Fall völlig klar.

Thema abgeschlossen.

Für mich allerdings nicht.

Ich kämpfte mich wieder raus aus dem Untergewicht, aber nichts hat sich dadurch verändert oder gar verbessert. Denn ich wusste, dass mit meinem Körper etwas nicht stimmt. Ich konnte es spüren.

6 Monate, seit ich mir eingestehen musste, dass mein altes Leben, so wie ich es kannte, nicht mehr existiert.

Der Versuch eine Balance zu finden zwischen Ärzte-Odyssee, Ausschlussdiagnostik und „das bildest du dir doch eh bloß ein“ Gedanken in meinem verdrehten Kopf.

3 Monate, seit ich einen anderen Arzt fand, der sich auskennt und vor allem: der mich ernst nahm.

1 Monat, seit der immunologischen Laboruntersuchung und den erschreckenden Ergebnissen mit erhöhten GPCR Autoantikörper, Interleukin Werten und dem eindeutigen Nachweis, einer Autoimmunreaktion.

3 Wochen, seit der offiziellen ME/CFS Diagnose meines Arztes, der von Anfang an wusste, dass ich zwar eine ganze Palette an psychischen Erkrankungen mitbringe, aber das akute Problem, eindeutig körperlicher Natur ist.

Seit dem. Steht alles still.

Denn mit der Diagnose, kam die Depression. Die nackte Angst, die pure Verzweiflung.

Nie war mein Blogname passender. Aber diesmal, gibt es kein Weg raus. Die auszeitstille, ist nicht mehr nur eine Auszeit. Die Stille wird bleiben, so lange, bis die Politik endlich hinsieht. Wir brauchen Forschung, Akzeptanz, Therapie und bitte bitte bitte irgendwann eine Heilung.

Egal wer das hier liest: bitte sieh hin, werde laut. Erkundige dich über ME/CFS, kläre auf und trage unsere Botschaft in die Welt hinaus. Wir sind sichtbar, wir wollen leben.

[emergencydrug]

Tofacitinib mechanism of action

Tofacitinib is a medication used to treat certain autoimmune diseases, primarily rheumatoid arthritis, psoriatic arthritis, and ulcerative colitis. Its mechanism of action involves targeting specific molecules and pathways in the immune system to reduce inflammation and modulate the immune response. Here's an overview of how tofacitinib works:

Janus Kinase (JAK) Inhibition: Tofacitinib drug belongs to a class of known as Janus Kinase (JAK) inhibitors. JAKs are enzymes that play a crucial role in transmitting signals within immune cells. By inhibiting specific JAK enzymes, tofacitinib interferes with the signaling pathways that lead to inflammation and immune system activation.

Cytokine Inhibition: JAK enzymes are involved in the signaling of various cytokines, which are small proteins that regulate immune responses. Tofacitinib primarily inhibits JAK1 and JAK3, which are associated with signaling by cytokines like interleukin-6 (IL-6), interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-7 (IL-7), interleukin-15 (IL-15), and interferon-gamma (IFN-gamma). By blocking these cytokine signals, tofacitinib helps reduce inflammation and control immune system activity.

Immune System Modulation: Tofacitinib helps modulate the immune response by reducing the activity of certain immune cells, particularly T cells and B cells, which are involved in autoimmune diseases. It can also affect other immune cells like natural killer (NK) cells and dendritic cells.

[medicomunicare]

Neuromyelitis optica "taken out of Breg": lymphocyte and cytokine signatures will grant the treatment conditions

No autoimmune diseases can currently be cured, only treated, and this is also true for neuromyelitis optica spectrum disorder (NEMOSD). Neuromyelitis optica disorder spectrum is one of them and it causes inflammation of the central nervous system, leading to vision and sensory loss, weakness and bladder dysfunction. The condition, which sometimes flares up in waves, has a treatment consisting of…

[vomitdodger]

From the article:

The American Academy of Pediatrics FALSELY states that “Vaccines are not associated with autism.”

Following is a list of abstracts from 212 papers demonstrating the multiple associations between vaccines and autism.

Autism is a largely immune mediated condition, and the purpose of a vaccine is to change the behavior of the immune system. Vaccines and their ingredients can cause the underlying medical conditions that are commonly found in children who have been given an autism diagnosis. These conditions include immune system impairment, autoimmune conditions, neuroinflammation, gastrointestinal damage, neurological regression, mitochondrial dysfunction, oxidative stress, glial cell activation, interleukin-6 secretion dysregulation, damage to the blood–brain barrier, seizures, dendritic cell dysfunction, mercury poisoning, aluminum toxicity, gene activation and alteration, glutathione depletion, impaired methylation, impaired thioredoxin regulation, impairment of the opioid system, cellular apoptosis, endocrine dysfunction, and other disorders.

[sommesick]

Autoimmune Registry adds Long COVID to its List of Diseases

The Autoimmune Registry has determined that biomarkers of immune system activity similar to those seen in many autoimmune and autoinflammatory diseases justify the inclusion of Long COVID on its list of diseases.

High levels of antibodies to the immune-system proteins called type I interferons (IFNs) have been associated with severe COVID-19.   Other studies have shown that severely ill patients tend to have a high concentration of pro-inflammatory cytokines, such as interleukin (IL)-6, compared to those who are moderately ill.

The Autoimmune Registry has decided to include Long COVID in its list of autoimmune diseases to support research into this emerging chronic condition.

[quirksphere]

Understanding Inflammatory Biomarkers: What They Are and Why They Matter

Inflammation is a natural process by which the body responds to injury, infection, or harmful stimuli. While it plays a crucial role in healing and defense, chronic or excessive inflammation can contribute to various diseases, such as cardiovascular disorders, diabetes, autoimmune conditions, and even cancer. To better understand and manage inflammation-related health conditions, researchers and healthcare providers rely on inflammatory biomarkers.

What Are Inflammatory Biomarkers?

Inflammatory biomarkers are measurable molecules in the blood, tissues, or other bodily fluids that indicate the presence or extent of inflammation in the body. These biomarkers are typically proteins, enzymes, or metabolites produced by the immune system or damaged tissues during an inflammatory response. By measuring their levels, healthcare providers can gain insights into a patient’s health status, track disease progression, or assess the effectiveness of treatments.

Types of Inflammatory Biomarkers

Inflammatory biomarkers can be broadly classified based on their origin or function. Some of the most commonly studied biomarkers include:

C-Reactive Protein (CRP): CRP is produced by the liver in response to inflammation. Elevated CRP levels are often associated with acute inflammation, infections, or chronic conditions like rheumatoid arthritis and cardiovascular disease.

Erythrocyte Sedimentation Rate (ESR): ESR measures how quickly red blood cells settle at the bottom of a test tube. A higher sedimentation rate can indicate inflammation or infection.

Cytokines: Cytokines are signaling proteins that regulate immune and inflammatory responses. Common pro-inflammatory cytokines include interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-alpha (TNF-α).

Fibrinogen: A protein involved in blood clotting, fibrinogen levels often rise during systemic inflammation and are linked to cardiovascular risk.

Serum Amyloid A (SAA): This acute-phase protein is produced in response to inflammatory signals and can serve as an indicator of infection or chronic inflammation.

Prostaglandins and Leukotrienes: These lipid molecules mediate inflammatory processes and are often studied in relation to asthma, arthritis, and other inflammatory conditions.

How Are Inflammatory Biomarkers Measured?

Inflammatory biomarkers are typically measured using blood tests, though some can be detected in saliva, urine, or tissue samples. Advanced laboratory techniques such as enzyme-linked immunosorbent assay (ELISA), mass spectrometry, and multiplex immunoassays are used to quantify these molecules with precision.

Clinical Applications of Inflammatory Biomarkers

Inflammatory biomarkers have a wide range of applications in medicine and research:

Disease Diagnosis and Monitoring: Elevated levels of certain biomarkers can help identify inflammatory or autoimmune conditions, such as lupus, rheumatoid arthritis, or inflammatory bowel disease. They are also used to monitor disease progression.

Cardiovascular Risk Assessment: High levels of CRP and fibrinogen are associated with an increased risk of heart attacks and strokes, making them valuable in assessing cardiovascular health.

Therapeutic Guidance: Biomarkers can help evaluate the effectiveness of anti-inflammatory medications, allowing for personalized treatment strategies.

Predicting Outcomes: In conditions like sepsis or COVID-19, elevated biomarkers such as IL-6 and CRP can predict disease severity and guide critical care interventions.

The Future of Inflammatory Biomarkers

Advances in genomics, proteomics, and bioinformatics are driving the discovery of novel inflammatory biomarkers. Researchers are exploring multi-biomarker panels that provide a more comprehensive picture of inflammation. Additionally, wearable technologies capable of monitoring biomarkers in real-time are on the horizon, promising to revolutionize how inflammation is tracked and managed.

Conclusion

Inflammatory biomarkers are powerful tools for understanding the body’s response to injury and disease. They offer invaluable insights into diagnosing, monitoring, and treating a wide range of conditions. As research progresses, these biomarkers will likely play an even greater role in precision medicine, helping to improve outcomes for patients worldwide. By staying informed about these advancements, both healthcare providers and patients can better navigate the complexities of inflammation-related health issues.

[infectiousdiseaseclinicaltrial]

COVID-19 Treatment Trials: Exploring the Path to Effective Therapeutics

The COVID-19 pandemic, caused by the SARS-CoV-2 virus, led to a global public health crisis that required urgent medical responses. As the virus rapidly spread across the world, the scientific community mobilized to find effective treatments to reduce the severity of illness and mortality rates. Clinical trials became the cornerstone of these efforts, helping to identify promising therapies that could alleviate symptoms, prevent disease progression, and ultimately save lives. In this article, we will review some key COVID-19 treatment trials and their findings, highlighting the innovations and challenges encountered during the race to find effective treatments.

Early Responses and Antiviral Trials

When COVID-19 first emerged in early 2020, one of the first areas of focus for clinical trials was the identification of existing antiviral medications that might be effective against SARS-CoV-2. Hydroxychloroquine, an antimalarial drug, became widely discussed as a potential treatment due to its ability to inhibit viral replication in laboratory settings.

Early observational studies and some small-scale trials indicated potential benefit, but larger, more rigorous clinical trials, such as the RECOVERY trial in the United Kingdom, ultimately showed no significant benefit of hydroxychloroquine for COVID-19 patients. This finding helped to clear the path for more evidence-based approaches. For more details visit https://www.infectiousdiseaseclinicaltrials.com/

Concurrently, the Solidarity trial, launched by the World Health Organization (WHO), evaluated several antiviral drugs, including remdesivir, lopinavir-ritonavir, and interferons. The trial found that while remdesivir showed modest benefits in reducing recovery time, it did not significantly reduce mortality rates. This result highlighted the challenges of finding an effective antiviral therapy for COVID-19, particularly given the virus's rapid mutation and ability to evade immune responses.

Steroid Treatments and Anti-inflammatory Approaches

One of the most impactful findings from clinical trials came in the form of dexamethasone, a corticosteroid. The RECOVERY trial, which tested a variety of treatments for COVID-19, demonstrated that dexamethasone, when administered to patients with severe disease or those requiring oxygen, reduced mortality by about one-third. Dexamethasone works by reducing inflammation, a key feature of severe COVID-19 infections, and it became one of the first widely accepted treatments for hospitalized patients.

Further studies focused on other anti-inflammatory approaches, such as interleukin-6 (IL-6) inhibitors like tocilizumab, which can block the inflammatory response associated with cytokine storms in severe COVID-19. Trials assessing these agents showed mixed results, but in some cases, particularly for patients requiring mechanical ventilation or those with high levels of inflammation, IL-6 inhibitors showed promise in improving outcomes.

Monoclonal Antibodies and Antibody-Based Therapies

Monoclonal antibodies (mAbs) represented another important avenue of COVID-19 treatment trials. These lab-engineered antibodies are designed to bind to specific parts of the SARS-CoV-2 virus, neutralizing its ability to infect cells. Several monoclonal antibodies, such as bamlanivimab and casirivimab-imdevimab, were authorized for emergency use in the U.S. after clinical trials demonstrated their ability to reduce the severity of illness in high-risk patients when administered early in the infection. However, as the virus evolved, with the emergence of variants like Delta and Omicron, some of these therapies became less effective, prompting the need for new monoclonal antibody formulations that target a broader range of viral strains.

Vaccine and Combination Therapies

While vaccines remain the most effective means of preventing severe COVID-19, combination therapies—utilizing antivirals, monoclonal antibodies, and corticosteroids together—have become an essential part of the treatment regimen for hospitalized patients. The ACTT-1 trial, which studied remdesivir in combination with other treatments, showed that the drug could shorten recovery time in hospitalized patients, particularly when used early in the infection.

Conclusion

The best COVID-19 treatment trials landscape has evolved rapidly, driven by the urgency of the pandemic and the collaborative efforts of the global medical and scientific communities. Through numerous clinical trials, researchers have identified effective strategies for managing the disease, such as corticosteroids, monoclonal antibodies, and antivirals.

While challenges remain, particularly with new viral variants, the lessons learned from these trials have not only informed COVID-19 treatment but have also paved the way for future therapeutic innovations in infectious disease management. As the pandemic continues to evolve, so too will our approach to treating COVID-19, ensuring that we are better prepared for both current and future health crises.

[covid-safer-hotties]

Reference preserved in our archive

Abstract Background: COVID-19 emerged in December 2019 and rapidly became a global pandemic. It has since been associated with the progression of various endocrine disorders, including thyroid disease. The long-term effects of this interplay have yet to be explored. This review explores the relationship between COVID-19 and thyroid diseases, emphasizing thyroid gland function and the clinical implications for managing thyroid disorders in infected individuals.

Objectives: This narrative review intends to provide insight into the scope of research that future clinical studies may aim to address regarding the long-term effects of COVID-19 infection on thyroid health.

Methods: Keywords including “thyroid disease”, “COVID-19”, and “long-term” were used to search PubMed and Google Scholar for updated and relevant clinical research.

Results: COVID-19 affects the thyroid gland multifacetedly and includes direct viral invasion, immune-mediated damage, and hypothalamic-pituitary-thyroid axis disruption. Approximately 15% of COVID-19 patients experience thyroid dysfunction, which can present as thyrotoxicosis, hypothyroidism, or non-thyroidal illness syndrome (NTI). Noteworthy findings include inflammatory thyroiditis. Long-term effects, including those observed in children, include persistent hypothyroidism and exacerbated pre-existing thyroid-autoimmune conditions. Management of thyroid disorders in COVID-19 patients requires consideration: anti-thyroid drug (ATD) therapy used to treat hyperthyroidism in COVID-19 patients may need adjustment to prevent immunosuppression. Radioactive iodine (ROI) alternatives and interleukin-6 (IL-6) receptor antagonists could offer potential benefits and should be further explored.

Conclusion: Longitudinal follow-ups post-COVID-19 for patients with new and pre-existing thyroid disorders can improve disease outcomes. In addition, pathophysiological research on thyroid dysfunction in COVID-19 may help develop strategies to prevent and alleviate thyroid gland abnormalities post-COVID-19.