Research unveils paths to stopping cytokine storms in COVID-19 JCI_Insight
Zhx2
hypomorph mice to model relapse of Minimal Change Disease , that improved after depletion of TNF-α or sIL-4Rα or IL-6. Thehypomorph state increased cell membrane to nuclear migration of podocyte ZHX proteins in vivo and lowered pSTAT6 activation in vitro.
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JCI Insight - Impaired PPARɣ activation by cadmium exacerbates infection-induced lung injury
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SARS-CoV-2 mRNA vaccines decouple anti-viral immunity from humoral autoimmunity - Nature CommunicationsWhilst SARS-CoV-2 mRNA vaccines have demonstrated efficacy in reducing infection severity, research has shown that SARS-CoV-2 infection is associated with new autoantibodies. Whether this would also be observed during mRNA vaccination is unclear. Here, the authors use an autoantibody screening platform to monitor autoantibody responses in a diverse cohort during vaccination.
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Can SARS-CoV-2 infection cause diabetes?This paper reports a population-based cohort study conducted in British Columbia, Canada, which found that SARS-CoV-2 infection is associated with a higher risk of diabetes, particularly among those with severe COVID-19 disease.
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Protein OCLN found to play crucial role in SARS-CoV-2 cell-to-cell transmissionResearch explains how the SARS-CoV-2 virus spreads efficiently by directly infecting neighboring cells through a process called cell-to-cell transmission. The virus uses a protein called occludin (OCLN) to enter the cells and causes syncytium formation, which leads to viral spread.
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Study gives insight into cause of severe inflammatory bowel diseaseCedars-Sinai investigators have identified a genetic variant that increases people's risk of developing perianal Crohn's disease, the most debilitating manifestation of Crohn's disease.
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Maternal exposure to ultrafine particles enhances influenza infection during pregnancy - Particle and Fibre ToxicologyBackground Interactions between air pollution and infectious agents are increasingly recognized and critical to identify, especially to protect vulnerable populations. Pregnancy represents a vulnerable period for influenza infection and air pollution exposure, yet interactions during pregnancy remain unclear. Maternal exposure to ultrafine particles (UFPs, $$\le$$ ≤ 100 nm diameter), a class of particulate matter ubiquitous in urban environments, elicits unique pulmonary immune responses. We hypothesized that UFP exposure during pregnancy would lead to aberrant immune responses to influenza enhancing infection severity. Results Building from our well-characterized C57Bl/6N mouse model employing daily gestational UFP exposure from gestational day (GD) 0.5–13.5, we carried out a pilot study wherein pregnant dams were subsequently infected with Influenza A/Puerto Rico/8/1934 (PR8) on GD14.5. Findings indicate that PR8 infection caused decreased weight gain in filtered air (FA) and UFP-exposed groups. Co-exposure to UFPs and viral infection led to pronounced elevation in PR8 viral titer and reduced pulmonary inflammation, signifying potential suppression of innate and adaptive immune defenses. Pulmonary expression of the pro-viral factor sphingosine kinase 1 (Sphk1) and pro-inflammatory cytokine interleukin-1β (IL-1 $$\beta$$ β ) was significantly increased in pregnant mice exposed to UFPs and infected with PR8; expression correlated with higher viral titer. Conclusions Results from our model provide initial insight into how maternal UFP exposure during pregnancy enhances respiratory viral infection risk. This model is an important first step in establishing future regulatory and clinical strategies for protecting pregnant women exposed to UFPs.
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