Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice

To investigate the influence of high salt on dextran sulfate sodium (DSS)-induced colitis in mice and explore the underlying mechanisms of this effect. DSS and NaCl were used to establish the proinflammatory animal model. We evaluated the colitis severity. Flow cytometry was employed for detecting t...

Full description

Saved in:
Bibliographic Details
Published in:World journal of gastroenterology : WJG 2018-04, Vol.24 (16), p.1779-1794
Main Authors: Guo, Hong-Xia, Ye, Nan, Yan, Ping, Qiu, Min-Yue, Zhang, Ji, Shen, Zi-Gang, He, Hai-Yang, Tian, Zhi-Qiang, Li, Hong-Li, Li, Jin-Tao
Format: Article
Language:English
Subjects:
Animals
Basic Study
Cells, Cultured
Colitis - chemically induced
Colitis - enzymology
Colitis - immunology
Colitis - pathology
Colon - drug effects
Colon - enzymology
Colon - immunology
Colon - pathology
Cytokines - genetics
Cytokines - metabolism
Dextran Sulfate
Disease Models, Animal
Female
Inflammation Mediators - metabolism
Intestinal Mucosa - drug effects
Intestinal Mucosa - enzymology
Intestinal Mucosa - immunology
Intestinal Mucosa - pathology
Macrophages, Peritoneal - drug effects
Macrophages, Peritoneal - immunology
Macrophages, Peritoneal - metabolism
MAP Kinase Signaling System - drug effects
Mice, Inbred C57BL
p38 Mitogen-Activated Protein Kinases - metabolism
Sodium Chloride - toxicity
T-Lymphocytes, Regulatory - drug effects
T-Lymphocytes, Regulatory - immunology
T-Lymphocytes, Regulatory - metabolism
Tissue Culture Techniques
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:To investigate the influence of high salt on dextran sulfate sodium (DSS)-induced colitis in mice and explore the underlying mechanisms of this effect. DSS and NaCl were used to establish the proinflammatory animal model. We evaluated the colitis severity. Flow cytometry was employed for detecting the frequencies of Th1, macrophages and Tregs in spleen, mesenteric lymph node and lamina propria. The important role of macrophages in the promotion of DSS-induced colitis by NaCl was evaluated by depleting macrophages with clodronate liposomes. Activated peritoneal macrophages and lamina propria mononuclear cells (LPMCs) were stimulated with NaCl, and proteins were detected by western blotting. Cytokines and inflammation genes were analyzed by enzyme-linked immunosorbent assay and RT-PCR, respectively. The study findings indicate that NaCl up-regulates the frequencies of CD11b macrophages and CD4 IFN-γ IL-17 T cells in lamina propria in DSS-treated mice. CD3 CD4 CD25 Foxp3 T cells, which can secrete high levels of IL-10 and TGF-β, increase through feedback in NaCl- and DSS-treated mice. Furthermore, clodronate liposomes pretreatment significantly alleviated DSS-induced colitis, indicating that macrophages play a vital role in NaCl proinflammatory activity. NaCl aggravates peritoneal macrophage inflammation by promoting the expressions of interleukin (IL)-1, IL-6 and mouse inducible nitric oxide synthase. Specifically, high NaCl concentrations promote p38 phosphorylation in lipopolysaccharide- and IFN-γ-activated LPMCs mediated by SGK1. Proinflammatory macrophages may play an essential role in the onset and development of NaCl-promoted inflammation in DSS-induced colitis. The underlining mechanism involves up-regulation of the p38/MAPK axis.
ISSN:1007-9327
2219-2840
DOI:10.3748/wjg.v24.i16.1779