Sex-Dependent Hepatoprotective Role of IL-22 Receptor Signaling in Non-Alcoholic Fatty Liver Disease-Related Fibrosis

Abdelnabi, Mohamed N.; Molina, Manuel Flores; Soucy, Geneviève; Trinh, Vincent Quoc‐Huy; Bédard, Nathalie; Mazouz, Sabrina; Jouvet, Nathalie; Dion, Jessica; Tran, Sarah; Bilodeau, Marc; Estall, Jennifer L.; Shoukry, Naglaa H.

doi:10.1016/j.jcmgh.2022.08.001

Cited by 9 publications

(8 citation statements)

References 68 publications

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“…Although Gunasekera et al’s work was based only on IL-10 −/− male mice between 16 to 20 weeks of age, studies have reported a significantly enhanced production of IL-22 in the liver of females compared to male mice [ 29 ]. Interestingly, testosterone seems to regulate IL-22 production in the female liver [ 29 ], playing sex-dependent immunosuppressive effects [ 30 ]. Estrogens, on another hand, have a complex role in inflammation and autoimmune disorders, with experimental evidence suggesting their involvement in gastrointestinal functions, potentially through estrogen receptor beta (ERβ).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Sex-Specific Differences on IL-10−/− Mouse Colitis Phenotype and Microbiota

Casado-Bedmar,

Roy,

Viennois

2023

IJMS

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Sexual dimorphism is an important factor in understanding various diseases, including inflammatory bowel disease (IBD). While females typically exhibit stronger immune responses, the role of sex in IBD remains unclear. This study aimed to explore the sex-dependent differences and inflammatory susceptibility in the most extensively used IBD mouse model as they developed colitis. We monitored IL10-deficient mice (IL-10−/−) up to 17 weeks of age and characterized their colonic and fecal inflammatory phenotype, as well as their microbiota changes. Here, we originally identified IL-10−/− female mice as more prone to developing intestinal inflammation, with an increase in fecal miR-21, and dysbiosis with more detrimental characteristics compared to males. Our findings provide valuable insights into the sex-based differences in the pathophysiology of colitis and emphasize the importance of considering sex in experimental designs. Moreover, this study paves the way for future investigations aiming at addressing sex-related differences for the development of adequate disease models and therapeutic strategies, ideally enabling personalized medicine.

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Section: Discussionmentioning

confidence: 99%

The Effect of Sex-Specific Differences on IL-10−/− Mouse Colitis Phenotype and Microbiota

Casado-Bedmar,

Roy,

Viennois

2023

IJMS

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“… 164 Abdelnabi et al. 165 demonstrated exacerbated liver damage, NASH-related inflammation, and apoptosis in female IL22ra1 −/− fed an HFD (40% kcal fat) for 30 weeks. Furthermore, the lack of IL22-receptor signaling promoted the progression of NASH-related fibrosis.…”

Section: Sex-based In Vivo Models Of Non-alcoholic...mentioning

confidence: 99%

“…Furthermore, the lack of IL22-receptor signaling promoted the progression of NASH-related fibrosis. 165 Using hepatocyte-specific Pten-deficient mice, Anezaki et al. 166 demonstrated that NAFL and inflammation were attenuated in females when compared to males.…”

Section: Sex-based In Vivo Models Of Non-alcoholic...mentioning

confidence: 99%

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Sex difference in liver diseases: How preclinical models help to dissect the sex-related mechanisms sustaining NAFLD and hepatocellular carcinoma

Smiriglia,

Lorito,

Serra

et al. 2023

iScience

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“…In obese mice, B. uniformis increased the expression of anti-inflammatory interleukin-22 (IL-22) and decreased the production of pro-inflammatory IFN associated with high-fat, high-sugar diet-induced liver damage, contributing to a greater balance of the hepatic immune status ( López-Almela et al, 2021 ). Notably, IL-22 has also shown a protective response to liver tissue injury, attenuating the inflammatory response in NAFLD models, and also alleviating oxidative stress, endoplasmic reticulum stress, and apoptosis ( Zai et al, 2021 ; Abdelnabi et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

Bacteroides and NAFLD: pathophysiology and therapy

Zhang,

Zhou,

et al. 2024

Front. Microbiol.

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Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic liver condition observed globally, with the potential to progress to non-alcoholic steatohepatitis (NASH), cirrhosis, and even hepatocellular carcinoma. Currently, the US Food and Drug Administration (FDA) has not approved any drugs for the treatment of NAFLD. NAFLD is characterized by histopathological abnormalities in the liver, such as lipid accumulation, steatosis, hepatic balloon degeneration, and inflammation. Dysbiosis of the gut microbiota and its metabolites significantly contribute to the initiation and advancement of NAFLD. Bacteroides, a potential probiotic, has shown strong potential in preventing the onset and progression of NAFLD. However, the precise mechanism by which Bacteroides treats NAFLD remains uncertain. In this review, we explore the current understanding of the role of Bacteroides and its metabolites in the treatment of NAFLD, focusing on their ability to reduce liver inflammation, mitigate hepatic steatosis, and enhance intestinal barrier function. Additionally, we summarize how Bacteroides alleviates pathological changes by restoring the metabolism, improving insulin resistance, regulating cytokines, and promoting tight-junctions. A deeper comprehension of the mechanisms through which Bacteroides is involved in the pathogenesis of NAFLD should aid the development of innovative drugs targeting NAFLD.

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Sex-Dependent Hepatoprotective Role of IL-22 Receptor Signaling in Non-Alcoholic Fatty Liver Disease-Related Fibrosis

Cited by 9 publications

References 68 publications

The Effect of Sex-Specific Differences on IL-10−/− Mouse Colitis Phenotype and Microbiota

The Effect of Sex-Specific Differences on IL-10−/− Mouse Colitis Phenotype and Microbiota

Sex difference in liver diseases: How preclinical models help to dissect the sex-related mechanisms sustaining NAFLD and hepatocellular carcinoma

Bacteroides and NAFLD: pathophysiology and therapy

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