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Impaired toll-like receptor signalling in peripheral B cells from newly diagnosed type-2 diabetic subjects.

ABSTRACT: Toll-like receptors (TLRs) under diabetic conditions trigger inflammation and impair immunity. In the present study, we looked at the expression of TLRs (2 and 4) and their adaptors in Normal Glucose Tolerant (NGT), Newly Diagnosed Type-2 Diabetic (NDD) and Known Type-2 Diabetic (KDM) subjects. We also estimated TLR induced cytokine secretion, cellular activation and apoptosis. Surface expression of TLR2 and 4 was significantly reduced in the B cells of the NDD subjects and was associated with decreased cellular activation and cytokine secretion (TNF-? and IL-6). This impairment was not due to B cell deficiency or apoptosis or immunosuppressive cytokine (IL-10 and TGF-?) secretion. However, the upregulation of immunomodulatory enzymes (Arg-1, HO-1 and IDO) could probably account for the reduced TLR expression. The defective TLR signalling was largely ameliorated in the KDM group which might be due to the use the anti-diabetic drugs which have anti-inflammatory effect.

SUBMITTER: Madhumitha H

PROVIDER: S-EPMC6367209 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature

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Impaired toll-like receptor signalling in peripheral B cells from newly diagnosed type-2 diabetic subjects.

Madhumitha Haridoss H Mohan Viswanathan V Kumar Nathella P NP Pradeepa Rajendra R Babu Subash S Aravindhan Vivekanandhan V

Cytokine 20150508 2

Toll-like receptors (TLRs) under diabetic conditions trigger inflammation and impair immunity. In the present study, we looked at the expression of TLRs (2 and 4) and their adaptors in Normal Glucose Tolerant (NGT), Newly Diagnosed Type-2 Diabetic (NDD) and Known Type-2 Diabetic (KDM) subjects. We also estimated TLR induced cytokine secretion, cellular activation and apoptosis. Surface expression of TLR2 and 4 was significantly reduced in the B cells of the NDD subjects and was associated with d ...[more]

PMID: 25959254

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Project description:AimThere are increasing evidence demonstrating that neutrophil-mediated inflammation plays a role in the etiology of type 2 diabetes. However, the molecular mechanisms by which neutrophils contribute to type 2 diabetes remain largely unknown. The aim of the present work was to identify possible changes in circulating neutrophils to better elucidate neutrophil involvement in human type 2 diabetes.MethodsPatients newly diagnosed with type 2 diabetes (n = 5) and age- and sex-matched healthy controls (n = 5) were recruited. Neutrophils were purified from type 2 diabetes patients and controls, and RNA sequencing (RNA-seq) was used for comprehensive transcriptome analysis. Differentially expressed genes (DEGs) were screened, and Gene Ontology (GO) and KEGG pathway enrichment analyses were performed. Real-time polymerase chain reaction (qPCR) was used for validation in external samples of type 2 diabetes patients (n = 8) and healthy controls (n = 8).ResultsGene expression analysis showed that, compared with neutrophils from healthy controls, there were 1990 upregulated DEGs and 1314 downregulated DEGs in neutrophils from type 2 diabetes patients. GO analysis demonstrated that the DEGs were mainly involved in myeloid leukocyte activation, T cell activation, adaptive immunity, and cytokine production. The top 20 enriched KEGG pathways included the cytokine-cytokine receptor interaction pathway, NF-?B signaling pathway, cell adhesion molecules, and chemokine signaling pathway. Furthermore, qPCR of genes related to neutrophil activation revealed that the expression of SELL, SELP, CXCR1, and S100A8 was significantly increased in neutrophils from type 2 diabetes patients compared with that in neutrophils from controls.ConclusionsOur study reveals an abnormal activation of circulating neutrophils at the transcriptome level in type 2 diabetes patients. These findings suggest a potential involvement of neutrophil dysfunction in the pathologic process of type 2 diabetes and provide insight into potential therapeutic targets for type 2 diabetes.

Dataset Information

Impaired toll-like receptor signalling in peripheral B cells from newly diagnosed type-2 diabetic subjects.

Publications

Impaired toll-like receptor signalling in peripheral B cells from newly diagnosed type-2 diabetic subjects.

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