Up-regulation of NHE8 by somatostatin ameliorates the diarrhea symptom in infectious colitis mice model
AffiliationUniv Arizona, Hlth Sci Ctr
MetadataShow full item record
CitationLei X, Cai L, Li X, Xu H, Geng C, Wang C. Up-regulation of NHE8 by somatostatin ameliorates the diarrhea symptom in infectious colitis mice model. Korean J Physiol Pharmacol. 2018 May;22(3):269-275. https://doi.org/10.4196/kjpp.2018.22.3.269
RightsCopyright © 2018 The Korean Physiological Society and The Korean Society of Pharmacology. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License.
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at firstname.lastname@example.org.
AbstractNa+/H+ exchangers (NHEs) have been shown to be involved in regulating cell volume and maintaining fluid and electrolyte homeostasis. Pooled evidences have suggested that loss of Na+/H+ exchanger isoform 8 (NHE8) impairs intestinal mucosa. Whether NHE8 participates in the pathology of infectious colitis is still unknown. Our previous study demonstrated that somatostatin (SST) could stimulate the expression of intestinal NHE8 so as to facilitate Na+ absorption under normal condition. This study further explored whether NHE8 participates in the pathological processes of infectious colitis and the effects of SST on intestinal NHE8 expression in the setting of infectious colitis. Our data showed that NHE8 expression was reduced in Citrobacter rodentium (CR) infected mice. Up-regulation of NHE8 improved diarrhea symptom and mucosal damage induced by CR. In vitro, a similar observation was also seen in Enteropathogenic E. coli (EPEC) infected Caco-2 cells. Seglitide, a SST receptor (SSTR) 2 agonist, partly reversed the inhibiting action of EPEC on NHE8 expression, but SSTR5 agonist (L-817,818) had no effect on the expression of NHE8. Moreover, SST blocked the phosphorylation of p38 in EPEC-infected Caco-2 cells. Taken together, these results suggest that enhancement of intestinal NHE8 expression by SST could ameliorate the symptoms of mice with infectious colitis.
NoteOpen Access Journal.
VersionFinal published version
SponsorsNational Natural Science Fund of China