Gut microbiota: sculptors of the intestinal stem cell niche in health and inflammatory bowel disease

Markandey, Manasvini; Bajaj, Aditya; Ilott, Nicholas E.; Kedia, Saurabh; Travis, Simon; Powrie, Fiona; Ahuja, Vineet

doi:10.1080/19490976.2021.1990827

Cited by 40 publications

(32 citation statements)

References 127 publications

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“…It has been reported that Paneth cells can sense microbial cues via TLR-Myd88 mediated pathways, in turn mounting antimicrobial defense by releasing antimicrobial peptides, lysozyme and phospholipase A. 38 Our results demonstrated that the microbiota structure was altered in TLR4ΔIEC mice, specifically the absence of Lactobacillus. L. reuteri was reported to be effective in promoting the number and function of Paneth cells to inhibit C. rodentium colonization.…”

Section: Discussionsupporting

confidence: 51%

Intestinal TLR4 deletion exacerbates acute pancreatitis through gut microbiota dysbiosis and Paneth cells deficiency

Mei

Huang

et al. 2022

Gut Microbes

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Toll-like receptor 4 (TLR4) has been identified as a potentially promising therapeutic target in acute pancreatitis (AP). However, the role of intestinal TLR4 in AP and AP-associated gut injury remains unclear. This study aimed to explore the relationship between intestinal TLR4 and gut microbiota during AP. A mouse AP model was establish by intraperitoneal injection of L-arginine. Pancreatic injury and intestinal barrier function were evaluated in wild-type and intestinal epithelial TLR4 knockout (TLR4ΔIEC) mice. Gut microbiota was analyzed by 16S rRNA sequencing. Quadruple antibiotics were applied to induce microbiota-depleted mice. Differentially expressed genes in gut were detected by RNA sequencing. L. reuteri treatment was carried out in vivo and vitro study. Compared with wild-type mice, AP and AP-associated gut injury were exacerbated in TLR4ΔIEC mice in a gut microbiota-dependent manner. The relative abundance of Lactobacillus and number of Paneth cells remarkably decreased in TLR4ΔIEC mice. The KEGG pathway analysis derived from RNA sequencing suggested that genes affected by intestinal TLR4 deletion were related to the activation of nod-like receptor pathway. Furthermore, L. reuteri treatment could significantly improve the pancreatic and intestinal injury in TLR4ΔIEC mice through promoting Paneth cells in a NOD2-dependent manner. Loss of intestinal epithelial TLR4 exacerbated pancreatic and intestinal damage during AP, which might be attributed to the gut microbiota dysbiosis especially the exhausted Lactobacillus. L. reuteri might maintain intestinal homeostasis and alleviate AP via Paneth cells modulation. Abbreviations: AP Acute pancreatitis, TLR4 Toll-like receptor 4, IL-1β Interleukin-1β, IL-6 Interleukin-6, TNF-α Tumor necrosis factor-α, SIRS Systematic inflammatory response syndrome, LPS Lipopolysaccharides, SPF Specific pathogen-free, ZO-1 Zonula occludens-1, CON Control, H&E Hematoxylin and eosin, FISH Fluorescence in situ hybridization, DAPI 4′,6-diamidino-2-phenylindole, PCoA Principal co-ordinates analysis, SCFA Short chain fatty acid, LEfSe Linear discriminant analysis Effect Size, ANOVA Analysis of variance, F/B Firmicutes/Bacteroidetes, PCA Principal component analysis, NOD2 Nod-like receptor 2, ABX antibiotics, PCNA proliferating cell nuclear antigen

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Section: Discussionsupporting

confidence: 51%

Intestinal TLR4 deletion exacerbates acute pancreatitis through gut microbiota dysbiosis and Paneth cells deficiency

Mei

Huang

et al. 2022

Gut Microbes

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“…If the butyrate-producing species in IBD patients is lost, it is observed that butyrate oxidation is impaired. On the basis off some researches, among the patients with IBD, the level of faecal SCFAs is reduced at different degrees[ 135 ]. This result is consistent with the research on the quantitative PCR targeting the butyryl-CoA: Acetate-CoA-transferase gene[ 136 ].…”

Section: Tryptophan Metabolismmentioning

confidence: 99%

Role of metabolites derived from gut microbiota in inflammatory bowel disease

Wen¹,

Duan²

2022

WJCC

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Over the past two decades, it is improved gut microbiota plays an important role in the health and disease pathogenesis. Metabolites, small molecules produced as intermediate or end products of microbial metabolism, is considered as one of the major interaction way for gut microbiota with the host. Bacterial metabolisms of dietary substrates, modification of host molecules or bacteria are the major source of metabolites. Signals from microbial metabolites affect immune maturation and homeostasis, host energy metabolism as well as mucosal integrity maintenance. Based on many researches, the composition and function of the microbiota can be changed, which is also seen in the metabolite profiles of patients with inflammatory bowel disease (IBD). Additionally, some specific classes of metabolites also can trigger IBD. In this paper, definition of the key classes of microbial-derived metabolites which are changed in IBD, description of the pathophysiological basis of association and identification of the precision therapeutic modulation in the future are the major contents.

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“…The intestinal microflora are members of this complex ecosystem, with more than 400 species of bacteria already identified [ 11 ]. Recent studies have found that intestinal microflora dysfunction can lead to intestinal inflammation and further lead to a range of diseases [ 12 , 13 ]. Some studies have also found that the metabolites of intestinal flora are involved in the key pathways that promote inflammation, fibrosis, and genotoxicity [ 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

An Extract of Artemisia argyi Leaves Rich in Organic Acids and Flavonoids Promotes Growth in BALB/c Mice by Regulating Intestinal Flora

Tan

Gong

et al. 2022

Animals

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In the context of global restrictions on the use of antibiotics, there has been increased research on natural plant-based ingredients as additives. It has been proved that many natural active ingredients contained in plants have positive effects on animal growth regulation. Artemisia argyi (A. argyi) is a traditional Chinese herbal medicine, and its extracts have been reported to have a variety of biological activities. Therefore, in order to explore the potential of the active extract of Artemisia argyi leaves (ALE) as a plant source additive, mice were fed with ALE at different concentrations for 60 days. Finally, the effects of ALE were evaluated by the growth indexes, blood indexes, and intestinal microflora changes of the mice. It was found that a medium concentration of ALE (150 mg/kg) could promote growth, and especially improved the feed efficiency of the mice. However, high concentrations of ALE (300 mg/kg) had some negative effects on the growth of mice, especially liver damage, which significantly increased AST and ALT levels in the blood. Therefore, the 150 mg/kg ALE treatment group was selected for 16S rDNA analysis. It was found that ALE could play a positive role by regulating the proportion of Bacteroidetes and Firmicutes in the intestinal tract. In particular, it can significantly up-regulate the quantities of Akkermansia and Bifidobacterium. These results suggest that ALE at appropriate concentrations can positively regulate animal growth.

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Gut microbiota: sculptors of the intestinal stem cell niche in health and inflammatory bowel disease

Cited by 40 publications

References 127 publications

Intestinal TLR4 deletion exacerbates acute pancreatitis through gut microbiota dysbiosis and Paneth cells deficiency

Intestinal TLR4 deletion exacerbates acute pancreatitis through gut microbiota dysbiosis and Paneth cells deficiency

Role of metabolites derived from gut microbiota in inflammatory bowel disease

An Extract of Artemisia argyi Leaves Rich in Organic Acids and Flavonoids Promotes Growth in BALB/c Mice by Regulating Intestinal Flora

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