ArticlemBio2015
Chronic superantigen exposure induces systemic inflammation, elevated bloodstream endotoxin, and abnormal glucose tolerance in rabbits: possible role in diabetes.
Article in mBio, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
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- The causal relationship between bacterial pneumonia and diabetes: a two-sample mendelian randomization study.Islets · 2024Article
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- Mediation Analysis of Waist Circumference in the Association of Gut Microbiota with Insulin Resistance in Children.Children (Basel, Switzerland) · 2023Article
- Microbiota and Glucidic Metabolism: A Link with Multiple Aspects and Perspectives.International journal of molecular sciences · 2023Review
- Pro- and anti-inflammatory bioactive lipids imbalance contributes to the pathobiology of autoimmune diseases.European journal of clinical nutrition · 2023Review
- Regulation of Staphylococcal Enterotoxin-Induced Inflammation in Spleen Cells from Diabetic Mice by Polyphenols.Microorganisms · 2023Article
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- Superantigens, a Paradox of the Immune Response.Toxins · 2022Review
- TSST-1The Journal of investigative dermatology · 2022Article
- Obesity Reshapes the Microbial Population Structure along the Gut-Liver-Lung Axis in Mice.Biomedicines · 2022Article
- The role of pathogens in diabetes pathogenesis and the potential of immunoproteomics as a diagnostic and prognostic tool.Frontiers in microbiology · 2022Review
- Effect of (-)-Epigallocatechin Gallate on Activation of JAK/STAT Signaling Pathway by Staphylococcal Enterotoxin A.Toxins · 2021Article
- Persistent SARS-2 infections contribute to long COVID-19.Medical hypotheses · 2021Article
- Kawasaki syndrome: role of superantigens revisited.The FEBS journal · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledExcessive weight and obesity are associated with the development of diabetes mellitus type 2 (DMII) in humans. They also pose high risks of Staphylococcus aureus colonization and overt infections. S. aureus causes a wide range of severe illnesses in both healthy and immunocompromised individuals. Among S. aureus virulence factors, superantigens are essential for pathogenicity. In this study, we show that rabbits that are chronically exposed to S. aureus superantigen toxic shock syndrome toxin-1 (TSST-1) experience impaired glucose tolerance, systemic inflammation, and elevated endotoxin levels in the bloodstream, all of which are common findings in DMII. Additionally, such DMII-associated findings are also seen through effects of TSST-1 on isolated adipocytes. Collectively, our findings suggest that chronic exposure to S. aureus superantigens facilitates the development of DMII, which may lead to therapeutic targeting of S. aureus and its superantigens. IMPORTANCE: Obesity has a strong correlation with type 2 diabetes, in which fatty tissue, containing adipocytes, contributes to the development of the illness through altered metabolism and chronic inflammation. The human microbiome changes in persons with obesity and type 2 diabetes, including increases in Staphylococcus aureus colonization and overt infections. While the microbiome is essential for human wellness, there is little understanding of the role of microbes in obesity or the development of diabetes. Here, we demonstrate that the S. aureus superantigen toxic shock syndrome toxin-1 (TSST-1), an essential exotoxin in pathogenesis, induces inflammation, lipolysis, and insulin resistance in adipocytes both in vitro and in vivo. Chronic stimulation of rabbits with TSST-1 results in impaired systemic glucose tolerance, the hallmark finding in type 2 diabetes in humans, suggesting a role of S. aureus and its superantigens in the progression to type 2 diabetes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.