scholarly journals Intestinal mesenchymal cells regulate immune responses and promote epithelial regeneration in vitro and in dextran sulfate sodium‐induced experimental colitis in mice

2021 ◽  
Author(s):  
Laura Hidalgo‐Garcia ◽  
José Alberto Molina‐Tijeras ◽  
Francisco Huertas‐Peña ◽  
Antonio Jesús Ruiz‐Malagón ◽  
Patricia Diez‐Echave ◽  
...  
2019 ◽  
Vol 13 (Supplement_1) ◽  
pp. S015-S015
Author(s):  
M Barnhoorn ◽  
L Plug ◽  
E Muller - de Jonge ◽  
E Bos ◽  
A van der Meulen - de Jong ◽  
...  

2017 ◽  
Vol 8 ◽  
Author(s):  
Zecai Zhang ◽  
Peng Shen ◽  
Xiaojie Lu ◽  
Yanxin Li ◽  
Jiuxi Liu ◽  
...  

RSC Advances ◽  
2015 ◽  
Vol 5 (112) ◽  
pp. 92008-92016 ◽  
Author(s):  
Hua Yu ◽  
Mingjun Dong ◽  
Yidong Xu ◽  
Ning He ◽  
Xiaoyu Dai ◽  
...  

This study aimed to investigate the effect and underlying mechanism of Arginyl-glutamine (AG) dipeptide on dextran sulfate sodium (DSS)-induced colitis byin vivoandin vitromodels.


1998 ◽  
Vol 31 (3) ◽  
pp. 477-481 ◽  
Author(s):  
Nahoko Shintani ◽  
Tsunetaka Nakajima ◽  
Tadao Okamoto ◽  
Takao Kondo ◽  
Norifumi Nakamura ◽  
...  

2020 ◽  
Vol 14 (10) ◽  
pp. 1462-1472 ◽  
Author(s):  
Danica Bajic ◽  
Adrian Niemann ◽  
Anna-Katharina Hillmer ◽  
Raquel Mejias-Luque ◽  
Sena Bluemel ◽  
...  

Abstract Background and Aims Regenerating islet-derived protein type 3 [Reg3] lectins are antimicrobial peptides at mucosal surfaces of the gut, whose expression is regulated by pathogenic gut microbes via interleukin-22- or Toll-like receptor signalling. In addition to antimicrobial effects, tissue protection is hypothesized, but has been poorly investigated in the gut. Methods We applied antibiotic-induced microbiota perturbations, gnotobiotic approaches and a dextran-sodium sulfate [DSS] colitis model to assess microbial Reg3 regulation in the intestines and its role in colitis. We also used an intestinal organoid model to investigate this axis in vitro. Results First, we studied whether gut commensals are involved in Reg3 expression in mice, and found that antibiotic-mediated reduction of Clostridia downregulated intestinal Reg3B. A loss in Clostridia was accompanied by a significant reduction of short-chain fatty acids [SCFAs], and knock-out [KO] mice for SCFA receptors GPR43 and GPR109 expressed less intestinal Reg3B/-G. Propionate was found to induce Reg3 in intestinal organoids and in gnotobiotic mice colonized with a defined, SCFA-producing microbiota. Investigating the role of Reg3B as a protective factor in colitis, we found that Reg3B-KO mice display increased inflammation and less crypt proliferation in the DSS colitis model. Propionate decreased colitis and increased proliferation. Treatment of organoids exposed to DSS with Reg3B or propionate reversed the chemical injury with a loss of expression of the stem-cell marker Lgr5 and Olfm4. Conclusions Our results suggest that Clostridia can regulate Reg3-associated epithelial homeostasis through propionate signalling. We also provide evidence that the Reg3–propionate axis may be an important mediator of gut epithelial regeneration in colitis.


2021 ◽  
Vol 49 (03) ◽  
pp. 661-676
Author(s):  
Yuanbing Zhu ◽  
Zhiqi Zhuang ◽  
Qiaofeng Wu ◽  
Sirui Lin ◽  
Na Zhao ◽  
...  

Ulcerative Colitis (UC) is a chronic inflammation disease, and the incidence of UC is increasing recently. Both clinical trials and animal experiments show that moxibustion is a complementary and alternative treatment for UC. Previous studies showed that moxibustion can improve UC by regulating the balance of Tregs and Th17 (Sun et al., 2017). Treg cells is one subset of CD4[Formula: see text] T cells that exert the immunosuppressive function. CD39 and CD73, expressed on the surface of Tregs, hydrolyze ATP to AMP and are further involved in the immunosuppressive function of Tregs. In this study, we investigated the effect of moxibustion on CD39[Formula: see text] Tregs and CD73[Formula: see text] Tregs in dextran sulfate sodium (DSS) induced UC mice. The A2a receptor (A2aR), one of the targets of adenosine, was also detected. The results showed that moxibustion could increase the expression of CD39, CD73, and A2aR in colonic tissue and improve the proportion of CD39[Formula: see text] Tregs and CD73[Formula: see text] Tregs in peripheral blood, inguinal draining lymph nodes and spleen in the UC model. Additionally, A2aR agonists enhanced the cell viability of colonic epithelial cells and inhibit the production of cytokines IL-6 and TNF-[Formula: see text] in vitro, which may further influence the pathway of ATP purine signal metabolism and alleviates the gut inflammation of UC mice. Taken together, this study provides supplemental evidence to reveal the immune related mechanism of moxibustion in the treatment of UC.


Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 7002
Author(s):  
Longlin Zhang ◽  
Mengmeng Ma ◽  
Zhengyi Li ◽  
Haihan Zhang ◽  
Xi He ◽  
...  

L-theanine is a nonprotein amino acid found in tea leaves and has been widely used as a safe food additive in beverages or foods because of its varied bioactivities. The aim of this study was to reveal the in vitro gastrointestinal protective effects of L-theanine in DSS-induced intestinal porcine enterocyte (IPEC-J2) cell models using molecular and metabolic methods. Results showed that 2.5% dextran sulfate sodium (DSS) treatment inhibited the cell proliferation of IPEC-J2 and blocked the normal operation of the cell cycle, while L-theanine pretreatment significantly preserved these trends to exert protective effects. L-theanine pre-treatment also up-regulated the EGF, CDC2, FGF2, Rb genes and down-regulated p53, p21 proliferation-related mRNA expression in DSS-treated cells, in accompany with p53 signaling pathway inhibition. Meanwhile, metabolomics analysis revealed that L-theanine and DSS treated IPEC-J2 cells have different metabolomic profiles, with significant changes in the key metabolites involved in pyrimidine metabolism and amino acid metabolism, which play an important role in nucleotide metabolism. In summary, L-theanine has a beneficial protection in DSS-induced IPEC-J2 cells via promoting proliferation and regulating metabolism disorders.


PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0159705 ◽  
Author(s):  
Toshihiro Kanda ◽  
Atsushi Nishida ◽  
Masashi Ohno ◽  
Hirotsugu Imaeda ◽  
Takashi Shimada ◽  
...  

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