scholarly journals Anti-Allergic Diarrhea Effect of Diosgenin Occurs via Improving Gut Dysbiosis in a Murine Model of Food Allergy

Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2471
Author(s):  
Chung-Hsiung Huang ◽  
Chorng-Liang Pan ◽  
Guo-Jane Tsai ◽  
Chun-Ju Chang ◽  
Wei-Chung Tsai ◽  
...  

Although the anti-allergic and prebiotic activities of diosgenin have been reported, the influence of diosgenin on intestinal immune and epithelial cells remains unclear. As the gut microbiota plays an important role in allergic disorders, this study aimed to investigate whether the anti-allergic diarrhea effect of diosgenin occurs via improving gut dysbiosis. In a murine food allergy model, the density of fecal bacterial growth on de Man, Rogossa and Sharpe (MRS) plates was diminished, and growth on reinforced clostridial medium (RCM) and lysogeny broth (LB) agar plates was elevated. However, the oral administration of diosgenin reduced the density of fecal bacteria and ameliorated diarrhea severity. Concordantly, reshaped diversity and an abundance of fecal microbes were observed in some of the diosgenin-treated mice, which showed a milder severity of diarrhea. The relevant fecal strains from the diosgenin-treated mice were defined and cultured with Caco-2 cells and allergen-primed mesenteric lymph node (MLN) cells. These strains exhibited protective effects against the cytokine/chemokine network and allergen-induced T-cell responses to varying degrees. By contrast, diosgenin limitedly regulated cytokine production and even reduced cell viability. Taken together, these findings show that diosgenin per se could not directly modulate the functionality of intestinal epithelial cells and immune cells, and its anti-allergic effect is most likely exerted via improving gut dysbiosis.

1997 ◽  
Vol 272 (4) ◽  
pp. G879-G884 ◽  
Author(s):  
P. E. Wischmeyer ◽  
M. W. Musch ◽  
M. B. Madonna ◽  
R. Thisted ◽  
E. B. Chang

Glutamine (Gln) protects gut mucosa against injury and promotes mucosal healing. Because the induction of heat shock proteins (HSP) protects cells under conditions of stress, we determined whether Gln conferred protection against stress in an intestinal epithelial cell line through HSP induction. Gln added to IEC-18 cells induces an increase in HSP70, a concentration-dependent effect also seen with mRNA. Two forms of injury, lethal heat (49 degrees C) and oxidant, were used, and viability was determined by 51Cr release. Gln-treated cells were significantly more resistant to injury. Treatment with 6-diazo-5-oxo-L-norleucine (DON), a nonmetabolizable analog of Gln, induced HSP70 and protected cells from injury, but less than Gln. These findings suggest that the effects of Gln on HSP70 induction and cellular protection are mediated by metabolic and nonmetabolic mechanisms. To determine whether HSP induction was central to the action of Gln and DON, quercetin, which blocks HSP induction, was used. Quercetin blocked HSP70 induction and the protective effect of Gln and DON. We conclude that the protective effects of Gln in intestinal epithelial cells are in part mediated by HSP70 induction.


2019 ◽  
Vol 54 (12) ◽  
pp. 2509-2513
Author(s):  
Jia Liu ◽  
Bo Li ◽  
Carol Lee ◽  
Haitao Zhu ◽  
Shan Zheng ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e104032 ◽  
Author(s):  
Xinwei Mu ◽  
Chen Pan ◽  
Shuyun Zheng ◽  
Yasir Alhamdi ◽  
Bingwei Sun ◽  
...  

2015 ◽  
Vol 59 (4) ◽  
pp. 698-710 ◽  
Author(s):  
Miriam Bermudez-Brito ◽  
Neha M. Sahasrabudhe ◽  
Christiane Rösch ◽  
Henk A. Schols ◽  
Marijke M. Faas ◽  
...  

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1513 ◽  
Author(s):  
Kang Xu ◽  
Yannan Guo ◽  
Lu Ping ◽  
Ying Qiu ◽  
Qingfei Liu ◽  
...  

Sirtuin 6 (SIRT6), as a NAD + -dependent deacetylase, plays an indispensable role in the regulation of health and physiology. Loss of SIRT6 causes spontaneous colitis in mice and makes intestinal epithelial cells prone to stress. However, whether SIRT6 overexpression increases resistance to colitis remains unknown. Here, in vivo results demonstrated that SIRT6 overexpression attenuates DSS-induced colitis in terms of clinical manifestations, histopathological damage, loss of tight junction function and imbalanced intestinal microenvironment. Additionally, we also found that the activation of NF-κB and c-Jun induced by DSS is diminished by SIRT6 overexpression. Furthermore, SIRT6 may regulate TAK1 to inhibit NF-κB and c-Jun signaling. Thus, our findings highlight the protective effect of SIRT6 on colon, further supporting the perspective that SIRT6 may be a therapeutic target for intestine injury under stress.


2019 ◽  
Vol 25 (4) ◽  
pp. 244-254 ◽  
Author(s):  
Han Gao ◽  
Bai-Sui Feng ◽  
Jiang-Qi Liu ◽  
Li-Hua Mo ◽  
Xiao-Rui Geng ◽  
...  

Survivin is an anti-apoptosis protein that may be associated with the development of eosinophilia; the latter is associated with the pathogenesis of many immune disorders. Here we report that less apoptotic eosinophils (Eos) were induced in those isolated from mice suffering from food allergy (FA) than those from naive mice after treating with cisplatin in vitro. Exposure to cisplatin induced more Fas ligand (FasL) expression in Eos isolated from naive mice than in those of FA mouse. Survivin was detected in the intestinal tissue extracts in much higher amounts in the FA group than in the naive group. Immunohistochemistry showed that epithelial cells were the major source of survivin in the intestine. Exposure to IL-4 or IL-13 up-regulated the expression of survivin in intestinal epithelial cells. Survivin interfered with the expression of FasL in Eos. Inhibition of survivin attenuated the eosinophilia-related inflammation in the intestine. In conclusion, intestinal epithelial cell-produced survivin induced defects in apoptosis in Eos to contribute to eosinophilia in the intestine. Inhibition of survivin can suppress the eosinophilia-related intestinal inflammation. The data suggest that survivin may be a novel target for the treatment of FA.


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