Inflammation induced ER stress affects absorptive intestinal epithelial cells function and integrity

Chotikatum, Sucheera; Naim, Hassan Y.; El‐Najjar, Nahed

doi:10.1016/j.intimp.2017.12.016

Cited by 35 publications

(28 citation statements)

References 87 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cx43 protein is abnormally expressed in the case of inflammation-induced intestinal epithelial cell injury (Chotikatum et al, 2018). Herein, Cx43 was colocalized with ZO-1 at the top of intestinal villi after MTX treatment, with enhanced fluorescence.…”

Section: Resultsmentioning

confidence: 99%

Protective Effects of Magnesium Glycyrrhizinate on Methotrexate-Induced Hepatotoxicity and Intestinal Toxicity May Be by Reducing COX-2

et al. 2019

View full text Add to dashboard Cite

Magnesium isoglycyrrhizinate (MgIG), which has been widely employed to treat chronic hepatitis, is synthesized from 18-β glycyrrhizic acid, a main component of traditional Chinese medicine Glycyrrhiza uralensis Fisch. Although the protective effects of MgIG on methotrexate (MTX)-induced liver toxicity have been well-documented, the underlying mechanism remains elusive. MTX was initially used to treat pediatric acute leukemia, and has been widely applied to psoriasis therapy. However, its clinical applications are limited due to hepatotoxicity and intestinal toxicity. Herein, prophylactic administration of MgIG (9 and 18 mg/kg/day) significantly reduced the levels of aspartate aminotransferase and alanine aminotransferase in the serum of rats receiving intravenous injection of MTX (20 mg/kg body weight). MgIG also attenuated MTX-induced hepatic fibrosis. Moreover, it better protected against MTX-induced hepatocyte apoptosis and decreased the serum level of malondialdehyde than reduced glutathione (80 mg/kg/day) did. Interestingly, MTX-induced cyclooxygenase-2 (COX-2) expression, intestinal permeability and inflammation were attenuated after MgIG administration. In addition, MgIG (9 and 18 mg/kg) reduced MTX-induced colocalization of zonula occludens-1 (ZO-1) and connexin 43 (Cx43) in intestinal villi. In conclusion, MgIG exerted beneficial effects on MTX-induced hepatotoxicity and intestinal damage, as a potentially eligible drug for alleviating the hepatic and intestinal side effects of MTX during chemotherapy.

show abstract

Section: Resultsmentioning

confidence: 99%

Protective Effects of Magnesium Glycyrrhizinate on Methotrexate-Induced Hepatotoxicity and Intestinal Toxicity May Be by Reducing COX-2

et al. 2019

View full text Add to dashboard Cite

show abstract

“…DPP-4 is a dipeptidyl peptidase localised in the brush border membrane, able to catabolise BCM-7 [ 52 ]. Inflammation, inducing the flattening of mucosal brush border, can cause the impairment of DPP-4 [ 53 ]. It is important to mention that Barnett and co-workers [ 9 ] measured DPP-4 activity after few days of milk feeding (36 to 84 h—acute model), while a longer milk consumption (30 days, in our study—chronic model) may probably result in a physiological attenuation of such an induction mechanism, which was reported, in any case, to not be mediated by a µ opioid signalling pathway.…”

Section: Discussionmentioning

confidence: 99%

A Comprehensive Evaluation of the Impact of Bovine Milk Containing Different Beta-Casein Profiles on Gut Health of Ageing Mice

et al. 2020

View full text Add to dashboard Cite

Ageing is often characterised by nutritional deficiencies and functional alterations of the digestive and immune system. The aim of the present study was to analyse the impact of consumption of conventional milk with A1/A2 beta-casein, compared to milk containing only the A2 beta-casein variant, characterised by a protein profile favouring gut health. Twenty-four ageing Balb-c mice (20 months old) were fed for 4 weeks, with either a control diet (CTRL), a diet supplemented with bovine milk containing A1/A2 beta-casein (A1A2) or a diet containing A2/A2 beta-casein (A2A2). Lymphocyte subpopulations, enzymatic activities, cytokine secretion, gut morphology and histopathological alterations were measured in different gut segments, while short-chain fatty acids (SCFAs) content and microbiota composition were evaluated in faecal samples. The A2A2 group showed higher content of faecal SCFAs (in particular, isobutyrate) of intestinal CD4+ and CD19+ lymphocytes in the intraepithelial compartment and improved villi tropism. The A1A2 group showed higher percentages of intestinal TCRγδ+ lymphocytes. Faecal microbiota identified Deferribacteriaceae and Desulfovibrionaceae as the most discriminant families for the A2A2 group, while Ruminococcaceae were associated to the A1A2 group. Taken together, these results suggest a positive role of milk, in particular when containing exclusively A2 beta-casein, on gut immunology and morphology of an ageing mice model.

show abstract

“…Severe burn has been documented to induce ER stress in some visceral organs, suggesting that ER stress is an important cellular response to burn injury and is associated with organ damage and dysfunction (Gauglitz et al., 2010; Jeschke et al., 2012; Song et al., 2014). ER stress was reported to be associated with intestinal epithelial dysfunction in inflammatory bowel disease (Kaser et al., 2010; Adolph et al., 2013; Cao, 2015; Luo and Cao, 2015; Chotikatum et al., 2018). Several clinical studies have also shown evidence for enhanced ER stress in the intestines of patients with inflammatory bowel disease (Hu et al., 2007; Shkoda et al., 2007; Kaser et al., 2008).…”

Section: Discussionmentioning

confidence: 99%

Role of Endoplasmic Reticulum Stress-Autophagy Axis in Severe Burn-Induced Intestinal Tight Junction Barrier Dysfunction in Mice

et al. 2019

View full text Add to dashboard Cite

Severe burn injury induces intestinal barrier dysfunction; however, the underlying mechanisms remain elusive. Our previous studies have shown that the intestinal epithelial tight junction (TJ) barrier dysfunction is associated with both endoplasmic reticulum (ER) stress and autophagy in severely burned mice, but the precise role of ER stress and autophagy in the burn-induced intestinal TJ barrier dysfunction needs to be determined. In this study, female C57/BL6 mice were assigned randomly to either sham burn or 30% total body surface area (TBSA) full-thickness burn. The effects of ER stress and autophagy on the intestinal epithelial TJ barrier were validated by inducing or inhibiting both ER stress and autophagy in mice treated with sham burn or burn injury. The intestinal permeability, expression, and localization of TJ proteins, ER stress, and autophagy were assessed by physiological, morphological, and biochemical analyses. The results showed that inducing ER stress with tunicamycin or thapsigargin caused the activation of autophagy, the increase of intestinal permeability, as well as the reduction and reorganization of TJ proteins in the sham-burned mice, and aggravated the burn-induced activation of autophagy, increase of intestinal permeability, as well as the reduction and reorganization of TJ proteins. In contrast, inhibiting ER stress with 4-phenylbutyrate alleviated the burn-induced activation of autophagy, increase of intestinal permeability, as well as the reduction and reorganization of TJ proteins. In addition, inducing autophagy with rapamycin resulted in the increase of intestinal permeability, as well as the reduction and reorganization of TJ proteins in the sham-burned mice, and aggravated the burn-induced increase of intestinal permeability as well as the reduction and reorganization of TJ proteins. However, inhibiting autophagy with 3-methyladenine attenuated the burn-induced increase of intestinal permeability, as well as the reduction and reorganization TJ proteins. It is suggested that the ER stress-autophagy axis contributes to the intestinal epithelial TJ barrier dysfunction after severe burn injury.

show abstract

Inflammation induced ER stress affects absorptive intestinal epithelial cells function and integrity

Cited by 35 publications

References 87 publications

Protective Effects of Magnesium Glycyrrhizinate on Methotrexate-Induced Hepatotoxicity and Intestinal Toxicity May Be by Reducing COX-2

Protective Effects of Magnesium Glycyrrhizinate on Methotrexate-Induced Hepatotoxicity and Intestinal Toxicity May Be by Reducing COX-2

A Comprehensive Evaluation of the Impact of Bovine Milk Containing Different Beta-Casein Profiles on Gut Health of Ageing Mice

Role of Endoplasmic Reticulum Stress-Autophagy Axis in Severe Burn-Induced Intestinal Tight Junction Barrier Dysfunction in Mice

Contact Info

Product

Resources

About