Dietary salt exacerbates intestinal fibrosis in chronic TNBS colitis via fibroblasts activation

Amamou, A.; Rouland, Matthieu; Yaker, Linda; Goichon, A.; Guérin, Charlène; Aziz, Moutaz; Savoye, Guillaume; Marion‐Letellier, Rachel

doi:10.1038/s41598-021-94280-8

Cited by 15 publications

(16 citation statements)

References 44 publications

(67 reference statements)

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“…56,59 In our study, there was no change in the expression of active calcium transport-related genes. As previously reported, this may be because the high-salt diet causes intestinal inflammation and fibrosis, 60–62 which may disrupt normal intestinal function and then cause 1,25(OH) 2 D 3 is failed to regulate the genes related to calcium transport. In more recent studies, paracellular Ca 2+ absorption was shown to be associated with the claudin protein family.…”

Section: Discussionmentioning

confidence: 84%

Calcitriol ameliorates damage in high-salt diet-induced hypertension: Evidence of communication with the gut–kidney axis

Ding

Xiao

Jiang

et al. 2021

Exp Biol Med (Maywood)

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Several studies have established a link between high-salt diet, inflammation, and hypertension. Vitamin D supplementation has shown anti-inflammatory effects in many diseases; gut microbiota is also associated with a wide variety of cardiovascular diseases, but potential role of vitamin D and gut microbiota in high-salt diet-induced hypertension remains unclear. Therefore, we used rats with hypertension induced by a high-salt diet as the research object and analyzed the transcriptome of their tissues (kidney and colon) and gut microbiome to conduct an overall analysis of the gut–kidney axis. We aimed to confirm the effects of high salt and calcitriol on the gut–kidney immune system and the composition of the intestinal flora. We demonstrate that consumption of a high-salt diet results in hypertension and inflammation in the colon and kidney and alteration of gut microbiota composition and function. High-salt diet-induced hypertension was found to be associated with seven microbial taxa and mainly associated with reduced production of the protective short-chain fatty acid butyrate. Calcitriol can reduce colon and kidney inflammation, and there are gene expression changes consistent with restored intestinal barrier function. The protective effect of calcitriol may be mediated indirectly by immunological properties. Additionally, the molecular pathways of the gut microbiota-mediated blood pressure regulation may be related to circadian rhythm signals, which needs to be further investigated. An innovative association analysis of the microbiota may be a key strategy to understanding the association between gene patterns and host.

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Section: Discussionmentioning

confidence: 84%

Calcitriol ameliorates damage in high-salt diet-induced hypertension: Evidence of communication with the gut–kidney axis

Ding

Xiao

Jiang

et al. 2021

Exp Biol Med (Maywood)

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“…Accordingly, a few studies using murine colitis models have observed that a high-salt diet exacerbates colitis, inducing an environment increasingly vulnerable to inflammatory insults [ 82 ]. Recently, we have characterised the effect of a high-salt diet on intestinal fibrogenesis using murine chronic colitis and cellular models of intestinal fibrosis [ 83 ]. Indeed, in our study, a high-salt diet increased mRNA transcripts encoding for pro-fibrotic markers, such as CTGF and collagen I, in chronic TNBS-induced colitis rats.…”

Section: Factors That Influence Macrophage Polarisation In Inflammati...mentioning

confidence: 99%

Gut Microbiota, Macrophages and Diet: An Intriguing New Triangle in Intestinal Fibrosis

et al. 2022

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Intestinal fibrosis is a common complication in inflammatory bowel disease (IBD) without specific treatment. As macrophages are the key actors in inflammatory responses and the wound healing process, they have been extensively studied in chronic diseases these past decades. By their exceptional ability to integrate diverse stimuli in their surrounding environment, macrophages display a multitude of phenotypes to underpin a broad spectrum of functions, from the initiation to the resolution of inflammation following injury. The hypothesis that distinct macrophage subtypes could be involved in fibrogenesis and wound healing is emerging and could open up new therapeutic perspectives in the treatment of intestinal fibrosis. Gut microbiota and diet are two key factors capable of modifying intestinal macrophage profiles, shaping their specific function. Defects in macrophage polarisation, inadequate dietary habits, and alteration of microbiota composition may contribute to the development of intestinal fibrosis. In this review, we describe the intriguing triangle between intestinal macrophages, diet, and gut microbiota in homeostasis and how the perturbation of this discreet balance may lead to a pro-fibrotic environment and influence fibrogenesis in the gut.

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“… 25 MiR-155 was demonstrated to directly target HMG-box transcription factor 1 and then activate Wnt/β-catenin signaling pathway, leading to intestinal fibrosis [ Figure 2(b) ]. 26 Amamou et al 30 reported that a high-salt diet also contributed to the activation of colon fibroblasts and intestinal fibrosis. The authors observed a significantly increased expression of fibrosis markers (e.g.…”

Section: Search Strategymentioning

confidence: 99%

Intestinal strictures in Crohn’s disease: a 2021 update

Lin

Wang

Liu

et al. 2022

Therap Adv Gastroenterol

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Intestinal strictures remain one of the most intractable and common complications of Crohn’s disease (CD). Approximately 70% of CD patients will develop fibrotic strictures after 10 years of CD diagnosis. Since specific antifibrotic therapies are unavailable, endoscopic balloon dilation and surgery remain the mainstay treatments despite a high recurrence rate. Besides, there are no reliable methods for accurately evaluating intestinal fibrosis. This is largely due to the fact that the mechanisms of initiation and propagation of intestinal fibrosis are poorly understood. There is growing evidence implying that the pathogenesis of stricturing CD involves the intricate interplay of factors including aberrant immune and nonimmune responses, host-microbiome dysbiosis, and genetic susceptibility. Currently, the progress on intestinal strictures has been fueled by the advent of novel techniques, such as single-cell sequencing, multi-omics, and artificial intelligence. Here, we perform a timely and comprehensive review of the substantial advances in intestinal strictures in 2021, aiming to provide prompt information regarding fibrosis and set the stage for the improvement of diagnosis, treatment, and prognosis of intestinal strictures.

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Dietary salt exacerbates intestinal fibrosis in chronic TNBS colitis via fibroblasts activation

Cited by 15 publications

References 44 publications

Calcitriol ameliorates damage in high-salt diet-induced hypertension: Evidence of communication with the gut–kidney axis

Calcitriol ameliorates damage in high-salt diet-induced hypertension: Evidence of communication with the gut–kidney axis

Gut Microbiota, Macrophages and Diet: An Intriguing New Triangle in Intestinal Fibrosis

Intestinal strictures in Crohn’s disease: a 2021 update

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