Mice born by C-section developed increased body weight and lacked microbiota developmental changes observed in control mice.

Background We studied risk factors, antibody responses, and symptoms of SARS-CoV-2 infection in a diverse, ambulatory population. Methods A prospective cohort (n=831, including 548 hospital-based healthcare workers) previously undiagnosed with SARS-CoV-2 infection was followed for six months with serial testing (SARS-CoV-2 PCR, specific IgG) and surveys. Results 93 participants (11.2%) tested SARS-CoV-2-positive; 14 (15.1%) were asymptomatic and 24 (25.8%), severely symptomatic. Healthcare workers were more likely to become infected (14.2% vs. 5.3%, aOR 2.1, 95% CI 1.4-3.3) and have severe symptoms (29.5% vs. 6.7%). IgG antibodies were detected after 79% of asymptomatic infections, 89% with mild-moderate symptoms, and 96% with severe symptoms. IgG trajectories after asymptomatic infection (slow increases) differed from symptomatic infections (early peaks within 2 months). Most participants (92%) had persistent IgG responses (median 171 days). In multivariable models, IgG titers were positively associated with symptom severity, certain comorbidities, and hospital work. Dyspnea, altered smell and taste, and other neurologic changes persisted for ≥120 days in ≥10% of affected participants. Participants with prolonged symptoms (generally more severely symptomatic) had higher antibody levels. Conclusions In a prospective, ethnically diverse cohort, symptom severity correlated with the magnitude and trajectory of IgG production. Symptoms frequently persisted for many months after infection.

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Type 1 diabetes (T1D) and Hashimoto's thyroiditis (HT) are the two most common autoimmune endocrine diseases that have rising global incidence. These diseases are caused by the immune-mediated destruction of hormone-producing endocrine cells, pancreatic beta cells and thyroid follicular cells, respectively. Both genetic predisposition and environmental factors govern the onset of T1D and HT. Recent evidence strongly suggests that the intestinal microbiota plays a role in accelerating or preventing disease progression depending on the compositional and functional profile of the gut bacterial communities. Accumulating evidence points towards the interplay between the disruption of gut microbial homeostasis (dysbiosis) and the breakdown of host immune tolerance at the onset of both diseases. In this review, we will summarize the major recent findings about the microbiome alterations associated with T1D and HT, and the connection of these changes to disease states. Furthermore, we will discuss the potential mechanisms by which gut microbial dysbiosis modulates the course of the disease, including disruption of intestinal barrier integrity and microbial production of immunomodulatory metabolites. The aim of this review is to provide broad insight into the role of gut microbiome in the pathophysiology of these diseases.