Enteric fungi protect against intestinal ischemia–reperfusion injury via inhibiting the SAA1-GSDMD pathway

Chen, Yihui; Han, Ben; Guan, Xu; Du, Guangsheng; Sheng, Baifa; Tang, Xiaoqi; Zhang, Quanchao; Xie, Huichao; Jiang, Xianhong; Tan, Qianshan; Chen, Shuaishuai; Wang, Jian; Chen, Wei; Xiao, Weidong

doi:10.1016/j.jare.2023.09.008

Cited by 5 publications

(3 citation statements)

References 69 publications

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“…The presence of tight junction molecules including claudin, occludin, and ZO-1 in intestinal tissues is essential for maintaining intestinal barrier function, as they are responsible for regulating paracellular permeability . In line with previous studies, , the intestinal I/R injury remarkably destroyed the intestinal structure, while the pretreatment of ABP1 significantly reduced the intestinal permeability via increasing the expression of ZO-1 and occludin. The improved intestinal barrier blocked the translocation of gut microbiota and their metabolites, such as LPS, preventing the activation of pattern recognition receptors including TLR2, TLR4, and NOD1, thereby alleviating infectious inflammation in intestinal tissues.…”

Section: Discussionsupporting

confidence: 84%

Polysaccharide Isolated from Agaricus blazei Murill Alleviates Intestinal Ischemia/Reperfusion Injury through Regulating Gut Microbiota and Mitigating Inflammation in Mice

Zhao,

Tang,

Huang

et al. 2024

J. Agric. Food Chem.

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Intestinal ischemia–reperfusion (I/R) injury is a serious disease in medical settings, and gut dysbiosis is a major contributor to its development. Polysaccharides from Agaricus blazei Murill (ABM) showed a range of pharmacological activities, yet no studies assessed the potential of ABM polysaccharides for alleviating intestinal I/R injury. Here, we purified a major polysaccharide (ABP1) from an ABM fruit body and subsequently tested its potential to mitigate intestinal I/R injury in a mouse model of temporary superior mesenteric artery occlusion. The results reveal that ABP1 pretreatment enhances gut barrier function via upregulation of the expression of tight junction proteins such as ZO-1 and occludin. Additionally, ABP1 intervention reduces the recruitment of neutrophils and the polarization of M1 macrophages and limits inflammation by blocking the assembly of the NLRP3 inflammasome. Moreover, the role of ABP1 in regulating the gut microbiota was confirmed via antibiotic treatment. The omics data reveals that ABP1 reprograms gut microbiota compositions, characterized by a decrease of Proteobacteria and an increase of Lachnospiraceae and Lactobacillaceae, especially the SCFA-producing genera such as Ligilactobacillus and Blautia. Overall, this work highlights the therapeutic potential of ABP1 against intestinal I/R injury, which mainly exhibits its effects via regulating the gut microbiota and suppressing the overactivated inflammation response.

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Section: Discussionsupporting

confidence: 84%

Polysaccharide Isolated from Agaricus blazei Murill Alleviates Intestinal Ischemia/Reperfusion Injury through Regulating Gut Microbiota and Mitigating Inflammation in Mice

Zhao,

Tang,

Huang

et al. 2024

J. Agric. Food Chem.

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“…For example, Saccharomyces boulardii exerts anti-pathogenic properties by upholding cellular physiology, obstructing the adherence of pathogens and their toxins, and engaging with the normal gut flora or aiding in the replenishment of short-chain fatty acid concentrations within the gut [6]. Furthermore, mono-colonization with Saccharomyces cerevisiae can alleviate intestinal ischemia-reperfusion injury by enhancing tight junction barrier function, reducing mucosal damage and epithelial permeability, and decreasing the release of inflammatory cytokines [7]. Nevertheless, should the fine balance between the immune system and symbiotic fungi be disturbed, the fungi may turn pathogenic, contributing to an array of disorders that include inflammatory bowel disease (IBD), hepatocellular carcinoma, and hypertension [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Gut Fungal Microbiota Alterations in Pulmonary Arterial Hypertensive Rats

Chen,

Meng,

Yuan

et al. 2024

Biomedicines

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The gut microbiome’s imbalance has been implicated in the pathogenesis of pulmonary arterial hypertension (PAH), yet the contribution of the gut mycobiome remains largely unclear. This study delineates the gut mycobiome profile in PAH and examines its interplay with the bacterial microbiome alterations. Fecal samples from monocrotaline-induced PAH rats and matched controls were subjected to internal transcribed spacer 1 (ITS1) sequencing for fungal community assessment and 16S ribosomal RNA (rRNA) gene sequencing for bacterial community characterization. Comparative analysis revealed no significant disparities in the overall mycobiome diversity between the PAH and control groups. However, taxonomic profiling identified differential mycobiome compositions, with the PAH group exhibiting a significant enrichment of genera such as Wallemia, unidentified_Branch02, Postia, Malassezia, Epicoccum, Cercospora, and Alternaria. Conversely, genera Xeromyces, unidentified_Plectosphaerellaceae, and Monilia were more abundant in the controls. Correlations of Malassezia and Wallemia abundance with hemodynamic parameters were observed. Indications of bidirectional fungal–bacterial community interactions were also noted. This investigation reveals distinct gut mycobiome alterations in PAH, which are intricately associated with concurrent bacterial microbiome changes, suggesting a possible contributory role of gut fungi in PAH pathophysiology. These findings underscore the potential for novel gut mycobiome-targeted therapeutic interventions in PAH management.

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“…Intestinal ischemia-reperfusion (IIR) injury is a common critical clinical condition, such as shock, intestinal obstruction, organ transplantation, extracorporeal circulation, and arterial embolism. 1 During ischemia, metabolic disorders associated with mitochondrial dysfunction and energy deficiency lead to intestinal injury; during reperfusion, excessive free radicals attack the cells that restore blood supply, resulting in further damage. IIR injury involves intestinal mucosal barrier damage, bacterial toxin translocation, microcirculation disorders, inflammatory storms, secondary inflammatory response syndromes, and even multiple organ dysfunction syndromes (MODS).…”

Section: Introductionmentioning

confidence: 99%

Ghrelin alleviates intestinal ischemia–reperfusion injury by activating the GHSR‐1α/Sirt1/FOXO1 pathway

Liao,

Zhang,

Zhang

et al. 2024

The FASEB Journal

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Ischemia–reperfusion (IR) injury is primarily characterized by the restoration of blood flow perfusion and oxygen supply to ischemic tissue and organs, but it paradoxically leads to tissue injury aggravation. IR injury is a challenging pathophysiological process that is difficult to avoid clinically and frequently occurs during organ transplantation, surgery, shock resuscitation, and other processes. The major causes of IR injury include increased levels of free radicals, calcium overload, oxidative stress, and excessive inflammatory response. Ghrelin is a newly discovered brain‐intestinal peptide with anti‐inflammatory and antiapoptotic effects that improve blood supply. The role and mechanism of ghrelin in intestinal ischemia–reperfusion (IIR) injury remain unclear. We hypothesized that ghrelin could attenuate IIR‐induced oxidative stress and apoptosis. To investigate this, we established IIR by using a non‐invasive arterial clip to clamp the root of the superior mesenteric artery (SMA) in mice. Ghrelin was injected intraperitoneally at a dose of 50 μg/kg 20 min before IIR surgery, and [D‐Lys3]‐GHRP‐6 was injected intraperitoneally at a dose of 12 nmol/kg 20 min before ghrelin injection. We mimicked the IIR process with hypoxia‐reoxygenation (HR) in Caco‐2 cells, which are similar to intestinal epithelial cells in structure and biochemistry. Our results showed that ghrelin inhibited IIR/HR‐induced oxidative stress and apoptosis by activating GHSR‐1α. Moreover, it was found that ghrelin activated the GHSR‐1α/Sirt1/FOXO1 signaling pathway. We further inhibited Sirt1 and found that Sirt1 was critical for ghrelin‐mediated mitigation of IIR/HR injury. Overall, our data suggest that pretreatment with ghrelin reduces oxidative stress and apoptosis to attenuate IIR/HR injury by binding with GHSR‐1α to further activate Sirt1.

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Enteric fungi protect against intestinal ischemia–reperfusion injury via inhibiting the SAA1-GSDMD pathway

Cited by 5 publications

References 69 publications

Polysaccharide Isolated from Agaricus blazei Murill Alleviates Intestinal Ischemia/Reperfusion Injury through Regulating Gut Microbiota and Mitigating Inflammation in Mice

Polysaccharide Isolated from Agaricus blazei Murill Alleviates Intestinal Ischemia/Reperfusion Injury through Regulating Gut Microbiota and Mitigating Inflammation in Mice

Gut Fungal Microbiota Alterations in Pulmonary Arterial Hypertensive Rats

Ghrelin alleviates intestinal ischemia–reperfusion injury by activating the GHSR‐1α/Sirt1/FOXO1 pathway

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