Metabolic Regulation of Group 3 Innate Lymphoid Cells and Their Role in Inflammatory Bowel Disease

Song, Dongjuan; Lai, Lijie; Ran, Zhihua

doi:10.3389/fimmu.2020.580467

Cited by 12 publications

(5 citation statements)

References 149 publications

(189 reference statements)

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“…But, due to the fact that only approximately 5% of SCFAs remain in faeces, there is no significant difference in the alterations in transit, absorption and utilization between the controlled subjects and healthy ones[ 138 ]. As a result, to know that anti-inflammatory associations with butyrateproducing bacteria may be caused by other mechanisms is also beneficial for the further study[ 139 ].…”

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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Section: Tryptophan Metabolismmentioning

confidence: 99%

Role of metabolites derived from gut microbiota in inflammatory bowel disease

Wen¹,

Duan²

2022

WJCC

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“…These modulations result in more thick mucus layer, which is an important property of intestinal homeostasis, giving a protective shield between epithelial cells and luminal bacteria ( Butzner et al, 1996 ; Segain et al, 2000 ; Geirnaert et al, 2017 ). Moreover, healthy diets represent a good source of aryl hydrocarbon receptor (AhR) which induce the production of IL-22, via the innate lymphoid cell 3 (ILC3) that maintains intestinal barrier function ( Song et al, 2020 ).…”

Section: Therapeutic Strategies Of Ibd Targeting Gut Microbiomementioning

confidence: 99%

Metabolic Influences of Gut Microbiota Dysbiosis on Inflammatory Bowel Disease

et al. 2021

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Inflammatory bowel diseases (IBD) are chronic medical disorders characterized by recurrent gastrointestinal inflammation. While the etiology of IBD is still unknown, the pathogenesis of the disease results from perturbations in both gut microbiota and the host immune system. Gut microbiota dysbiosis in IBD is characterized by depleted diversity, reduced abundance of short chain fatty acids (SCFAs) producers and enriched proinflammatory microbes such as adherent/invasive E. coli and H2S producers. This dysbiosis may contribute to the inflammation through affecting either the immune system or a metabolic pathway. The immune responses to gut microbiota in IBD are extensively discussed. In this review, we highlight the main metabolic pathways that regulate the host-microbiota interaction. We also discuss the reported findings indicating that the microbial dysbiosis during IBD has a potential metabolic impact on colonocytes and this may underlie the disease progression. Moreover, we present the host metabolic defectiveness that adds to the impact of symbiont dysbiosis on the disease progression. This will raise the possibility that gut microbiota dysbiosis associated with IBD results in functional perturbations of host-microbiota interactions, and consequently modulates the disease development. Finally, we shed light on the possible therapeutic approaches of IBD through targeting gut microbiome.

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“…Altered Th17/Treg balance in obesity, T2D, and NAFLD * [85] ↑pro-inflammatory cytokines in DIO mice [86,87] ↑IL-17-producing γδ T cells [87,88] and ↑IFN-γ-producing Th1 and CD8 + T cells [87] in DIO mice ↓IL-22 in db/db, ob/ob, and DIO mice [89] ↓Tregs in DIO mice * [85][86][87]89,90] ↓eosinophils in DIO mice [91] Altered Th1/Th2 [92], Th1/Th17 [93,94], Th1/Treg [95] and/or Th17/Treg balance [92,94,95] in IBD * ↑Th1 responses (↑IFN-γ) in CD * [96,97] ↑Th2 responses (↑IL-4 and IL-5) in UC * [96,98] ↑Th17 (↑IL-17, IL-21, and IL-22) in IBD * [99] ↑Th1 or Th17 responses (↑IFN-γ and IL-17) in CD, and↑NK T (↑IL-13), IL-4, IL-5 in UC [98,100] ↑Th1-like Th17 (↑IFN-γ and IL-17), T17-like Treg in CD [101] ↑Th1-like Treg (↑IFN-γ) in both CD and UC [102] ↑plasticity of ILC3s (NKp44 + NKp46 + ) to ILC1s (NKp44 − NKp46 − ) and ↑plasticity of ILC2s to ILC1s in CD [103,104] ↓ILCreg in IBD [105,106] * Possible links between metabolic disorders and IBD.…”

Section: Intestinal Immune Dysfunctionmentioning

confidence: 99%

“…Regulatory ILCs (ILCreg), a recently identified subset of ILCs, which appear to be distinct from Treg cells due to the lack of expression of CD4 and FoxP3 [130], have also been found to contribute to maintaining intestinal homeostasis and protecting against inflammation through generating IL-10 and TGF-β, thereby suppressing the production of IFN-γ and IL-17A by ILC1 and NCR − ILC3, respectively [105]. Dysregulated activation of ILCregs could be linked to an impairment of regulatory anti-inflammatory function in the innate immunity, leading to the development of IBD [106].…”

Section: Intestinal Pro-inflammatory State Induced By Ibdmentioning

confidence: 99%

Molecular and Pathophysiological Links between Metabolic Disorders and Inflammatory Bowel Diseases

Hyun

2021

IJMS

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Despite considerable epidemiological evidence indicating comorbidity between metabolic disorders, such as obesity, type 2 diabetes, and non-alcoholic fatty liver disease, and inflammatory bowel diseases (IBD), such as Crohn’s disease and ulcerative colitis, as well as common pathophysiological features shared by these two categories of diseases, the relationship between their pathogenesis at molecular levels are not well described. Intestinal barrier dysfunction is a characteristic pathological feature of IBD, which also plays causal roles in the pathogenesis of chronic inflammatory metabolic disorders. Increased intestinal permeability is associated with a pro-inflammatory response of the intestinal immune system, possibly leading to the development of both diseases. In addition, dysregulated interactions between the gut microbiota and the host immunity have been found to contribute to immune-mediated disorders including the two diseases. In connection with disrupted gut microbial composition, alterations in gut microbiota-derived metabolites have also been shown to be closely related to the pathogeneses of both diseases. Focusing on these prominent pathophysiological features observed in both metabolic disorders and IBD, this review highlights and summarizes the molecular risk factors that may link between the pathogeneses of the two diseases, which is aimed at providing a comprehensive understanding of molecular mechanisms underlying their comorbidity.

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Metabolic Regulation of Group 3 Innate Lymphoid Cells and Their Role in Inflammatory Bowel Disease

Cited by 12 publications

References 149 publications

Role of metabolites derived from gut microbiota in inflammatory bowel disease

Role of metabolites derived from gut microbiota in inflammatory bowel disease

Metabolic Influences of Gut Microbiota Dysbiosis on Inflammatory Bowel Disease

Molecular and Pathophysiological Links between Metabolic Disorders and Inflammatory Bowel Diseases

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