ArticlePloS one2009
The toll-like receptor signaling molecule Myd88 contributes to pancreatic beta-cell homeostasis in response to injury.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- TRAF6 integrates innate immune signals to regulate glucose homeostasis via Parkin-dependent and Parkin-independent mitophagy.Science advances · 2025Article
- Glucagon-like Peptide 1 Receptor Agonists in Cardio-Oncology: Pathophysiology of Cardiometabolic Outcomes in Cancer Patients.International journal of molecular sciences · 2024Review
- The role of innate immunity in diabetic nephropathy and their therapeutic consequences.Journal of pharmaceutical analysis · 2024Review
- Inhibition of hyaluronan synthesis prevents β-cell loss in obesity-associated type 2 diabetes.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- Divalent Metal Transporter 1 Knock-Down Modulates IL-1β Mediated Pancreatic Beta-Cell Pro-Apoptotic Signaling Pathways through the Autophagic Machinery.International journal of molecular sciences · 2021Article
- Crosstalk between Macrophages and Pancreatic β-Cells in Islet Development, Homeostasis and Disease.International journal of molecular sciences · 2021Review
- Toll-like Receptors as a Potential Drug Target for Diabetes Mellitus and Diabetes-associated Complications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Review
- Hyaluronan content governs tissue stiffness in pancreatic islet inflammation.The Journal of biological chemistry · 2018Article
- Differential role of MyD88 and TRIF signaling in myeloid cells in the pathogenesis of autoimmune diabetes.PloS one · 2018Article
- TCDD influences reservoir of antibiotic resistance genes in murine gut microbiome.FEMS microbiology ecology · 2017Article
- Mitochondrial DNA Activates the NLRP3 Inflammasome and Predisposes to Type 1 Diabetes in Murine Model.Frontiers in immunology · 2017Article
- Gut microbiome in chronic kidney disease: challenges and opportunities.Translational research : the journal of laboratory and clinical medicine · 2017Review
- Gut microbiota translocation to the pancreatic lymph nodes triggers NOD2 activation and contributes to T1D onset.The Journal of experimental medicine · 2016Article
- Innate immunity in diabetes and diabetic nephropathy.Nature reviews. Nephrology · 2016Review
- Inhibition of hyaluronan synthesis restores immune tolerance during autoimmune insulitis.The Journal of clinical investigation · 2015Article
- Blowing on embers: commensal microbiota and our immune system.Frontiers in immunology · 2014Review
- 'Blooming' in the gut: how dysbiosis might contribute to pathogen evolution.Nature reviews. Microbiology · 2013Review
- The biodiversity hypothesis and allergic disease: world allergy organization position statement.The World Allergy Organization journal · 2013Article
- Lysine 63-linked ubiquitination modulates mixed lineage kinase-3 interaction with JIP1 scaffold protein in cytokine-induced pancreatic β cell death.The Journal of biological chemistry · 2013Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Commensal flora and pathogenic microbes influence the incidence of diabetes in animal models yet little is known about the mechanistic basis of these interactions. We hypothesized that Myd88, an adaptor molecule in the Toll-like-receptor (TLR) pathway, regulates pancreatic beta-cell function and homeostasis. We first examined beta-cells histologically and found that Myd88-/- mice have smaller islets in comparison to C57Bl/6 controls. Myd88-/- mice were nonetheless normoglycemic both at rest and after an intra-peritoneal glucose tolerance test (IPGTT). In contrast, after low-dose streptozotocin (STZ) challenge, Myd88-/-mice had an abnormal IPGTT relative to WT controls. Furthermore, Myd88-/- mice suffer enhanced beta-cell apoptosis and have enhanced hepatic damage with delayed recovery upon low-dose STZ treatment. Finally, we treated WT mice with broad-spectrum oral antibiotics to deplete their commensal flora. In WT mice, low dose oral lipopolysaccharide, but not lipotichoic acid or antibiotics alone, strongly promoted enhanced glycemic control. These data suggest that Myd88 signaling and certain TLR ligands mediate a homeostatic effect on beta-cells primarily in the setting of injury.
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Registered trials
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.