Histamine Causes Pyroptosis of Liver by Regulating Gut-Liver Axis in Mice

Luo, Qiaoqiao; Shi, Ruoyu; Liu, Yutong; Huang, Libo; Chen, Wei; Wang, Chengtao

doi:10.3390/ijms23073710

Cited by 10 publications

(5 citation statements)

References 39 publications

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“…In addition, YEH was able to reduce the content of histamine in this pathway, which mediates GI tract damage that is induced by alcohol ( Zimatkin and Anichtchik, 1999 ). Studies in mouse models have found that the oral administration of histamine can cause gut microbiota disorder, oxidative stress, inflammatory response ( Luo et al, 2022 ), and cause liver fibrosis ( Kennedy et al, 2020 ). In morphine addiction and cGMP-PKG signaling pathways, high doses of yeast extract modulate both pathways by reducing the levels of adenosine and 5′ -adenine nucleotide ( Figure 7B ).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of yeast extract against alcohol-induced liver injury in rats

Lin

Wang

et al. 2023

Front. Microbiol.

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Oxidative stress, inflammatory response, and gut-liver axis dysbiosis have been suggested as the primarily involved in the pathogenesis of alcoholic liver injury. Previous research established that yeast extract (YE) has antioxidant, immune-boosting or microbiota-regulating properties. However, there is currently lack of information regarding the efficacy of YE on alcoholic liver injury. This study seeks to obtain data that will help to address this research gap using a Wistar male rat experimental model. Histologic and biochemical analysis results showed that the groups treated with both low-dose yeast extract (YEL) and high-dose yeast extract (YEH) had lower degrees of alcohol-induced liver injury. The abundance of Peptococcus and Ruminococcus reduced in the low-dose yeast extract (YEL) group, while that of Peptococcus, Romboutsia, Parasutterella, and Faecalibaculum reduced in the high-dose (YEH) group. Furthermore, Spearman analysis showed that the gut microbes were significantly associated with several liver-related indicators. For the analysis of differential metabolites and enriched pathways in the YEL group, the abundance of lysophosphatidylcholine (16:0/0:0) significantly increased, and then the levels of histamine, adenosine and 5′ -adenine nucleotide were remarkedly elevated in the YEH group. These findings suggest that both high and low doses of YE can have different protective effects on liver injury in alcoholic liver disease (ALD) rats, in addition to improving gut microbiota disorder. Besides, high-dose YE has been found to be more effective than low-dose YE in metabolic regulation, as well as in dealing with oxidative stress and inflammatory responses.

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Section: Discussionmentioning

confidence: 99%

Protective effects of yeast extract against alcohol-induced liver injury in rats

Lin

Wang

et al. 2023

Front. Microbiol.

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“…The presence of bile acid in the intestine contributes to a normal gut barrier function by promoting intestinal epithelial cell proliferation. In biliary obstruction, intestinal mucosal injury is mainly due to more LPS caused by intestinal flora disorder ( Assimakopoulos et al, 2007 ; Luo et al, 2022 ). To further confirm the effect of OCA on the proliferation and apoptosis of intestinal mucosal epithelial cells, Caco2 cells were incubated with LPS and OCA in vitro .…”

Section: Resultsmentioning

confidence: 99%

Effects of Intestinal FXR-Related Molecules on Intestinal Mucosal Barriers in Biliary Tract Obstruction

Yan

Cai

et al. 2022

Front. Pharmacol.

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Background: The farnesoid X receptor (FXR) is a key factor regulating hepatic bile acid synthesis and enterohepatic circulation. Repression of bile acid synthesis by the FXR is a potential strategy for treating cholestatic liver disease. However, the role of intestinal FXR on the intestinal barrier and intestinal microbiota needs further investigation.Materials: Intestinal tissues were collected from patients with biliary atresia or without hepatobiliary disease. Then, intestinal mRNA levels of FXR-related molecules were determined. To investigate the effect of FXR activation, bile-duct-ligation rats were treated with obeticholic acid [OCA (5 mg/kg/day)] or vehicle (0.5% methyl cellulose) per oral gavage for 14 days. The mRNA levels of intestinal FXR, SHP, TNF-α, FGF15 and bile acid transporter levels were determined. In addition, the intestinal permeability, morphologic changes, and composition of the intestinal microbiota were evaluated. Gut Microbiome was determined by 16S rDNA MiSeq sequencing, and functional profiling of microbial communities was predicted with BugBase and PICRUSt2. Finally, the role of OCA in injured intestinal epithelial cell apoptosis and proliferation was examined by pretreatment with lipopolysaccharide (LPS) in Caco-2 cells.Results: The downstream of the FXR in ileum tissues was inhibited in biliary obstruction. Activation of the FXR signaling pathway by OCA significantly reduced liver fibrosis and intestinal inflammation, improved intestinal microbiota, and protected intestinal mucosa in BDL rats. OCA also altered the functional capacities of ileum microbiota in BDL rats. Significant differences existed between the controls and BDL rats, which were attenuated by OCA in the alpha diversity analysis. Principal coordinates analysis showed that microbial communities in BDL rats clustered separately from controls, and OCA treatment attenuated the distinction. Bugbase and PICRUSt2 analysis showed that OCA changed the composition and structure of the intestinal microbiota and improved the metabolic function of the intestinal microbiota by increasing the relative abundance of beneficial bacteria and reducing the relative abundance of harmful bacteria. Moreover, OCA reduced the apoptosis induced by LPS in Caco-2 cells.Conclusion: The FXR agonist, OCA, activates the intestinal FXR signaling pathway and improves the composition and structure of the intestinal microbiota and intestinal barrier in BDL rats.

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“…Pearson’s correlation analysis showed that the relative abundance of microbiota relating to liver pyroptosis, e.g., Parabacteroides , Bacteroides , Lactobacillus , and Alistipes , were increased significantly in AFB 1 -treated mice, as well as in the transplanted group. Several lines of evidence indicated that Parabacteroides , Bacteroides , and Alistipes could activate NLRP3 signaling. The variation of these gut bacteria is consistent with the activation of liver pyroptosis, indicating that they could be the key factors to promote liver pyroptosis.…”

Section: Discussionmentioning

confidence: 99%

Aflatoxin B₁ Induces Inflammatory Liver Injury via Gut Microbiota in Mice

Chen

Tsim

et al. 2023

J. Agric. Food Chem.

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Aflatoxin B 1 (AFB 1 ), a potent food-borne hepatocarcinogen, is the most toxic aflatoxin that induces liver injury in humans and animals. Species-specific sensitivities of aflatoxins cannot be fully explained by differences in the metabolism of AFB 1 between animal species. The gut microbiota are critical in inflammatory liver injury, but it remains to reveal the role of gut microbiota in AFB 1 -induced liver injury. Here, mice were gavaged with AFB 1 for 28 days. Then, the modulation of gut microbiota, colonic barrier, and liver pyroptosis and inflammation were analyzed. To further verify the direct role of gut microbiota in AFB 1induced liver injury, mice were treated with antibiotic mixtures (ABXs) to deplete the microbiota, and fecal microbiota transplantation (FMT) was conducted. The treatment of AFB 1 in mice altered gut microbiota composition, such as increasing the relative abundance of Bacteroides, Parabacteroides, and Lactobacillus, inducing colonic barrier dysfunction and promoting liver pyroptosis. In ABX-treated mice, AFB 1 had little effect on the colonic barrier and liver pyroptosis. Notably, after FMT, in which the mice were colonized with gut microbiota from AFB 1 -treated mice, colonic barrier dysfunction, and liver pyroptosis and inflammation were obliviously identified. We proposed that the gut microbiota directly participated in AFB 1 -induced liver pyroptosis and inflammation. These results provide new insights into the mechanisms of AFB 1 hepatotoxicity and pave a window for new targeted interventions to prevent or reduce AFB 1 hepatotoxicity.

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Histamine Causes Pyroptosis of Liver by Regulating Gut-Liver Axis in Mice

Cited by 10 publications

References 39 publications

Protective effects of yeast extract against alcohol-induced liver injury in rats

Protective effects of yeast extract against alcohol-induced liver injury in rats

Effects of Intestinal FXR-Related Molecules on Intestinal Mucosal Barriers in Biliary Tract Obstruction

Aflatoxin B₁ Induces Inflammatory Liver Injury via Gut Microbiota in Mice

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Histamine Causes Pyroptosis of Liver by Regulating Gut-Liver Axis in Mice

Cited by 10 publications

References 39 publications

Protective effects of yeast extract against alcohol-induced liver injury in rats

Protective effects of yeast extract against alcohol-induced liver injury in rats

Effects of Intestinal FXR-Related Molecules on Intestinal Mucosal Barriers in Biliary Tract Obstruction

Aflatoxin B1 Induces Inflammatory Liver Injury via Gut Microbiota in Mice

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Product

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Aflatoxin B₁ Induces Inflammatory Liver Injury via Gut Microbiota in Mice