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Helicobacter pylori infection downregulates duodenal CFTR and SLC26A6 expressions through TGFβ signaling pathway

Overview of attention for article published in BMC Microbiology, August 2018
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Title
Helicobacter pylori infection downregulates duodenal CFTR and SLC26A6 expressions through TGFβ signaling pathway
Published in
BMC Microbiology, August 2018
DOI 10.1186/s12866-018-1230-8
Pubmed ID
Authors

Guorong Wen, Shili Deng, Wenfeng Song, Hai Jin, Jingyu Xu, Xuemei Liu, Rui Xie, Penghong Song, Biguang Tuo

Abstract

The pathogenesis of Helicobacter pylori (H. pylori) infection-induced duodenal ulcer remains to be elucidated. Duodenal mucosal bicarbonate secretion is the most important protective factor against acid-induced mucosal injury. We previously revealed that H. pylori infection downregulated the expression and functional activity of duodenal mucosal cystic fibrosis transmembrane conductance regulator (CFTR) and solute linked carrier 26 gene family A6 (SLC26A6) which are the two key duodenal mucosal epithelial cellular bicarbonate transporters to mediate duodenal bicarbonate secretion. In this study, we investigated the mechanism of H. pylori infection-induced duodenal CFTR and SLC26A6 expression downregulation. We found that H. pylori infection induced the increase of serum transforming growth factor β (TGFβ) level and duodenal mucosal TGFβ expression and the decrease of duodenal mucosal CFTR and SLC26A6 expressions in C57 BL/6 mice. The results from the experiments of human duodenal epithelial cells (SCBN) showed that H. pylori increased TGFβ production and decreased CFTR and SLC26A6 expressions in SCBN cells. TGFβ inhibitor SB431542 reversed the H. pylori-induced CFTR and SLC26A6 expression decreases. The further results showed that TGFβ directly decreased CFTR and SLC26A6 expressions in SCBN cells. TGFβ induced the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and P38 MAPK inhibitor SB203580 reversed the TGFβ-induced CFTR and SLC26A6 expression decreases. H. pylori infection downregulates duodenal epithelial cellular CFTR and SLC26A6 expressions through TGFβ-mediated P38 MAPK signaling pathway, which contributes to further elucidating the pathogenesis of H. pylori-associated duodenal ulcer.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 23 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 23 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 5 22%
Other 4 17%
Student > Bachelor 3 13%
Student > Postgraduate 2 9%
Student > Ph. D. Student 1 4%
Other 2 9%
Unknown 6 26%
Readers by discipline Count As %
Medicine and Dentistry 6 26%
Biochemistry, Genetics and Molecular Biology 4 17%
Immunology and Microbiology 4 17%
Agricultural and Biological Sciences 1 4%
Nursing and Health Professions 1 4%
Other 1 4%
Unknown 6 26%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 19 August 2018.
All research outputs
#20,530,891
of 23,100,534 outputs
Outputs from BMC Microbiology
#2,708
of 3,216 outputs
Outputs of similar age
#290,349
of 333,251 outputs
Outputs of similar age from BMC Microbiology
#48
of 55 outputs
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So far Altmetric has tracked 3,216 research outputs from this source. They receive a mean Attention Score of 4.1. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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