Helicobacter pylori -derived heat shock protein 60 increases the induction of regulatory T-cells associated with persistent infection

Hsu, Wei Tung; Ho, Shu Yi; Jian, Ting Yan; Huang, Han Ning; Lin, Yuling; Chen, Chia-Hung; Lin, Tsung H.; Wu, Ming Shiang; Wu, Chang Jer; Chan, Yi Lin; Liao, Kuang‐Wen

doi:10.1016/j.micpath.2018.04.016

Cited by 13 publications

(10 citation statements)

References 47 publications

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“…HspA60-mediated inflammation within the gastric mucosa is due to its interactions with the TLR and further overactivation of the NF-κB, ERK, and MAP kinase (MAPK) signaling pathways with a subsequent IL-8 and TNF-α secretion from the monocytic cells [364][365][366][367]. Macrophages are stimulated by Hsp60 to release the IL-6 due to the overactivation of the NF-κB pathway as well as IL-10 and TGF-β that stimulate the proliferation of Treg cells promoting inflammation [368,369]. Furthermore, Hsp60 is involved in H. pylori adherence and further colonization within the gastric epithelium.…”

Section: Heat Shock Proteinsmentioning

confidence: 99%

Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment

Baj

Forma

Sitarz

et al. 2020

Cells

222

163

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Gastric cancer constitutes one of the most prevalent malignancies in both sexes; it is currently the fourth major cause of cancer-related deaths worldwide. The pathogenesis of gastric cancer is associated with the interaction between genetic and environmental factors, among which infection by Helicobacter pylori (H. pylori) is of major importance. The invasion, survival, colonization, and stimulation of further inflammation within the gastric mucosa are possible due to several evasive mechanisms induced by the virulence factors that are expressed by the bacterium. The knowledge concerning the mechanisms of H. pylori pathogenicity is crucial to ameliorate eradication strategies preventing the possible induction of carcinogenesis. This review highlights the current state of knowledge and the most recent findings regarding H. pylori virulence factors and their relationship with gastric premalignant lesions and further carcinogenesis.

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Section: Heat Shock Proteinsmentioning

confidence: 99%

Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment

Baj

Forma

Sitarz

et al. 2020

Cells

222

163

View full text Add to dashboard Cite

show abstract

“…In addition to affecting the function of intestinal epithelial cells, H. pylori could modulate the role of immune cells in the intestinal tract. A previous study suggested that H. pylori led to the upregulation of heat shock protein 60 in macrophages to promote TGF-β production, which contributed to the infiltration of regulatory T cells (Treg) to cause persistent infection[38]. Clinical data showed an increased number of Treg in children with H. pylori infection, and TGF-β had a positive correlation with the increase of Treg[39].…”

Section: Disccusionmentioning

confidence: 99%

MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori

Feng¹,

Guo²,

Wang³

et al. 2019

WJG

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BACKGROUNDPediatric enteritis is one of the infectious diseases in the digestive system that causes a variety of digestive problems, including diarrhea, vomiting, and bellyache in children. Clinically, Helicobacter pylori (H. pylori) infection is one of the common factors to cause pediatric enteritis. It has been demonstrated that aberrant expression of microRNAs (miRNAs) is found in gastrointestinal diseases caused by H. pylori, and we discovered a significant increase of miR-32-5p in H. pylori-related pediatric enteritis. However, the exact role of miR-32-5p in it is still unknown.AIMTo investigate the role of aberrant miR-32-5p in pediatric enteritis induced by H. pylori.METHODSMiR-32-5p expression was detected by quantitative real time-polymerase chain reaction. The biological role of miR-32-5p in H. pylori-treated intestinal epithelial cells was evaluated by Cell Counting Kit-8 assay and flow cytometry. The potential target of miR-32-5p was predicted with TargetScanHuman and verified by luciferase assay. The downstream mechanism of miR-32-5p was explored by using molecular biology methods.RESULTSWe found that miR-32-5p was overexpressed in serum of H. pylori-induced pediatric enteritis. Further investigation revealed that H. pylori infection promoted the death of intestinal epithelial cells, and increased miR-32-5p expression. Moreover, miR-32-5p mimic further facilitated apoptosis and inflammatory cytokine secretion of intestinal epithelial cells. Further exploration revealed that SMAD family member 6 (SMAD6) was the direct target of miR-32-5p, and SMAD6 overexpression partially rescued cell damage induced by H. pylori. The following experiments showed that miR-32-5p/SMAD6 participated in the apoptosis of intestinal epithelial cells induced by transforming growth factor-β-activated kinase 1 (TAK1)-p38 activation under H. pylori infection.CONCLUSIONOur work uncovered the crucial role of aberrant expression of miR-32-5p in H. pylori–related pediatric enteritis, and suggested that the TAK1-p38 pathway is involved in it.

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“…L. rhamnosus JB-1 EVs were also enriched in heat shock proteins (HSPs) ( 177 ), a highly conserved protein family across species. HSP are critical regulators of Treg via TLR2 ( 178 ) with HSPs from E. coli ( 179 ), Mycobacterium tuberculosis ( 180 , 181 ), H. pylori ( 182 ), as well as from helminths ( 183 ) promoting Treg in vitro . Treg specific for bacterial HSP can also recognize host HSP, which are released during inflammation.…”

Section: Gut Bacterial Metabolites and Ptreg Developmentmentioning

confidence: 99%

Your Regulatory T Cells Are What You Eat: How Diet and Gut Microbiota Affect Regulatory T Cell Development

et al. 2022

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Modern industrial practices have transformed the human diet over the last century, increasing the consumption of processed foods. Dietary imbalance of macro- and micro-nutrients and excessive caloric intake represent significant risk factors for various inflammatory disorders. Increased ingestion of food additives, residual contaminants from agricultural practices, food processing, and packaging can also contribute deleteriously to disease development. One common hallmark of inflammatory disorders, such as autoimmunity and allergies, is the defect in anti-inflammatory regulatory T cell (Treg) development and/or function. Treg represent a highly heterogeneous population of immunosuppressive immune cells contributing to peripheral tolerance. Tregs either develop in the thymus from autoreactive thymocytes, or in the periphery, from naïve CD4+ T cells, in response to environmental antigens and cues. Accumulating evidence demonstrates that various dietary factors can directly regulate Treg development. These dietary factors can also indirectly modulate Treg differentiation by altering the gut microbiota composition and thus the production of bacterial metabolites. This review provides an overview of Treg ontogeny, both thymic and peripherally differentiated, and highlights how diet and gut microbiota can regulate Treg development and function.

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Helicobacter pylori -derived heat shock protein 60 increases the induction of regulatory T-cells associated with persistent infection

Cited by 13 publications

References 47 publications

Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment

Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment

MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori

Your Regulatory T Cells Are What You Eat: How Diet and Gut Microbiota Affect Regulatory T Cell Development

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