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


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-08-17

AUTHORS

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

ABSTRACT

BackgroundThe 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.ResultsWe 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.ConclusionsH. 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. More... »

PAGES

87

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URI

http://scigraph.springernature.com/pub.10.1186/s12866-018-1230-8

DOI

http://dx.doi.org/10.1186/s12866-018-1230-8

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https://app.dimensions.ai/details/publication/pub.1106156024

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30119655


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38 Further results
39 H. pylori infection
40 H. pylori-associated duodenal ulcer
41 Helicobacter pylori infection
42 MAPK
43 MAPK inhibitor SB203580
44 ResultsWe
45 SB203580
46 SCBN cells
47 SLC26A6 expression
48 TGFβ
49 TGFβ expression
50 TGFβ production
51 acid-induced mucosal injury
52 activity
53 bicarbonate secretion
54 bicarbonate transporters
55 cells
56 conductance regulator
57 cystic fibrosis transmembrane conductance regulator
58 decrease
59 downregulation
60 duodenal bicarbonate secretion
61 duodenal epithelial cells
62 duodenal mucosal bicarbonate secretion
63 duodenal ulcer
64 epithelial cells
65 experiments
66 expression
67 expression decreases
68 expression downregulation
69 factors
70 fibrosis transmembrane conductance regulator
71 functional activity
72 growth factor β levels
73 human duodenal epithelial cells
74 important protective factor
75 increase
76 infection
77 inhibitor SB203580
78 inhibitors
79 injury
80 kinase
81 levels
82 mechanism
83 mice
84 mitogen
85 mucosal bicarbonate secretion
86 mucosal injury
87 p38 MAPK
88 p38 MAPK inhibitor SB203580
89 p38 mitogen
90 pathogenesis
91 pathway
92 phosphorylation
93 production
94 protective factors
95 protein kinase
96 pylori infection
97 regulator
98 results
99 secretion
100 solutes
101 study
102 transmembrane conductance regulator
103 transporters
104 ulcers
105 β levels
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