Indole-3-propionic Acid Improved the Intestinal Barrier by Enhancing Epithelial Barrier and Mucus Barrier

Li, Jiaojiao; Zhang, Li; Wu, Tao; Li, Yafei; Zhou, Xiaojun; Ruan, Zheng

doi:10.1021/acs.jafc.0c05205

Cited by 125 publications

(91 citation statements)

References 41 publications

(71 reference statements)

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“… 2 IPA is similar in structure to melatonin. More and more studies have confirmed the beneficial effects of IPA on the intestines 30 and liver, 15 which are mainly manifested in stabilizing the intestinal mucosal barrier, regulating the intestinal flora, and interacting with the immune system to change intestinal biology properties, such as anti-inflammatory and anti-oxidant. Although previous research has proposed subtle differences in the chemical structure between melatonin and IPA and speculated the latter substance may have unfavorable effects, 10 , 17 , 18 there are no relevant reports so far.…”

Section: Discussionmentioning

confidence: 96%

Indole-3-propionic Acid-aggravated CCl4-induced Liver Fibrosis via the TGF-β1/Smads Signaling Pathway

Liu¹,

Sun²,

Chen³

et al. 2021

Journal of Clinical and Translational Hepatology

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Background and Aims:The pathogenesis of liver fibrosis involves liver damage, inflammation, oxidative stress, and intestinal dysfunction. Indole-3-propionic acid (IPA) has been demonstrated to have antioxidant, anti-inflammatory and anticancer activities, and a role in maintaining gut homeostasis. The current study aimed to investigate the role of IPA in carbon tetrachloride (CCl 4 )-induced liver fibrosis and explore the underlying mechanisms. Methods: The liver fibrosis model was established in male C57BL/6 mice by intraperitoneal injection of CCl 4 twice weekly. IPA intervention was made orally (20 mg/kg daily). The degree of liver injury and fibrosis were assessed by serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and histopathology. Enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction (qPCR) were used to detect the inflammatory cytokines. The malondialdehyde (MDA), glutathione, glutathione peroxidase, superoxide dismutase, and catalase were determined via commercial kits. Hepatocyte apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay. The expression of mRNA and protein was assayed by qPCR, Western blotting, or immunohistochemical staining. Results: After IPA treatment, the ALT and AST, apoptotic cells, and pro-inflammatory factor levels were enhanced significantly. Moreover, IPA intervention up-regulated the expression of collagen I, α-smooth muscle actin, tissue inhibitor of matrix metalloproteinase-1, matrix metalloproteinase-2, transforming growth factor-β1 (TGF-β1), Smad3, and phosphorylated-Smad2/3. Additionally, IPA intervention did not affect the MDA level. Attrac-tively, the administration of IPA remodeled the gut flora structure. Conclusions: IPA aggravated CCl 4 -induced liver damage and fibrosis by activating HSCs via the TGF-β1/ Smads signaling pathway.

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Section: Discussionmentioning

confidence: 96%

Indole-3-propionic Acid-aggravated CCl4-induced Liver Fibrosis via the TGF-β1/Smads Signaling Pathway

Liu¹,

Sun²,

Chen³

et al. 2021

Journal of Clinical and Translational Hepatology

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“…85 Feeding rats a high-fat diet damages the epithelial barrier, which is reversed by IPA treatment via increased Muc2 and Muc4 expression, which strengthen the mucosal layer. 86,87 In addition, IPA also up-regulates MUC2 expression in a colonic spheroid culture system. 88 A combination of Trp and Lactobacillus plantarum KLDS 1.0386 (high Trp-metabolic activity) treatment improved the epithelial and mucus barrier by decreasing the expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) in adextran sodium sulfate (DSS)-induced colitis mouse model.…”

Section: Tryptophan Metabolitementioning

confidence: 99%

Mucins, gut microbiota, and postbiotics role in colorectal cancer

et al. 2021

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An imbalance in the crosstalk between the host and gut microbiota affects the intestinal barrier function, which results in inflammatory diseases and colorectal cancer. The colon epithelium protects itself from a harsh environment and various pathogenic organisms by forming a double mucus layer, primarily comprising mucins. Recent studies are focusing on how dietary patterns alter the gut microbiota composition, which in turn regulates mucin expression and maintains the intestinal layers. In addition, modulation of gut microbiota by microbiotic therapy (involving fecal microbiota transplantation) has emerged as a significant factor in the pathologies associated with dysbiosis. Therefore, proper communication between host and gut microbiota via different dietary patterns (prebiotics and probiotics) is needed to maintain mucus composition, mucin synthesis, and regulation. Here, we review how the interactions between diet and gut microbiota and bacterial metabolites ( postbiotics ) regulate mucus layer functionalities and mucin expression in human health and disease.

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“…GF-mice colonization with an IPA-producing strain like C. sporogenes restores the IPA serum level [ 13 ]. It was shown to activate the AhR and the PXR pathways leading to the reduction of the symptoms in a mice-dextran sodium sulfate (DSS) model of colitis [ 157 , 158 ]. Thus, IPA might be an interesting candidate for the treatment of UC.…”

Section: Microbiota-derived Metabolites That Modulate Host Immunity In the Gutmentioning

confidence: 99%

What We Know So Far about the Metabolite-Mediated Microbiota-Intestinal Immunity Dialogue and How to Hear the Sound of This Crosstalk

et al. 2021

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Trillions of microorganisms, termed the “microbiota”, reside in the mammalian gastrointestinal tract, and collectively participate in regulating the host phenotype. It is now clear that the gut microbiota, metabolites, and intestinal immune function are correlated, and that alterations of the complex and dynamic host-microbiota interactions can have deep consequences for host health. However, the mechanisms by which the immune system regulates the microbiota and by which the microbiota shapes host immunity are still not fully understood. This article discusses the contribution of metabolites in the crosstalk between gut microbiota and immune cells. The identification of key metabolites having a causal effect on immune responses and of the mechanisms involved can contribute to a deeper insight into host-microorganism relationships. This will allow a better understanding of the correlation between dysbiosis, microbial-based dysmetabolism, and pathogenesis, thus creating opportunities to develop microbiota-based therapeutics to improve human health. In particular, we systematically review the role of soluble and membrane-bound microbial metabolites in modulating host immunity in the gut, and of immune cells-derived metabolites affecting the microbiota, while discussing evidence of the bidirectional impact of this crosstalk. Furthermore, we discuss the potential strategies to hear the sound of such metabolite-mediated crosstalk.

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Indole-3-propionic Acid Improved the Intestinal Barrier by Enhancing Epithelial Barrier and Mucus Barrier

Cited by 125 publications

References 41 publications

Indole-3-propionic Acid-aggravated CCl4-induced Liver Fibrosis via the TGF-β1/Smads Signaling Pathway

Indole-3-propionic Acid-aggravated CCl4-induced Liver Fibrosis via the TGF-β1/Smads Signaling Pathway

Mucins, gut microbiota, and postbiotics role in colorectal cancer

What We Know So Far about the Metabolite-Mediated Microbiota-Intestinal Immunity Dialogue and How to Hear the Sound of This Crosstalk

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