1.Bacteroides fragilis alleviates necrotizing enterocolitis through restoring bile acid metabolism balance using bile salt hydrolase and inhibiting FXR-NLRP3 signaling pathway

https://pubmed.ncbi.nlm.nih.gov/39013030/

DOI:10.1080/19490976.2024.2379566

Necrotizing enterocolitis (NEC) is an inflammatory bowel disease that can progress to intestinal necrosis and sepsis, and is a major cause of morbidity and mortality among neonates in intensive care units. Currently, there is no specific treatment for NEC. This study primarily aims to determine the molecular mechanisms of NEC and to investigate the therapeutic effects of Bacteroides fragilis on NEC. According to the preliminary conclusions of the article, Bacteroides fragilis exhibits therapeutic potential by inhibiting the FXR-NLRP3 signaling pathway, restoring intestinal dysbiosis, and correcting abnormal bile acid metabolism. It demonstrates the presence of the bsh gene and enzyme activity, thereby alleviating intestinal injury. For further details, please refer to the original article.

2.Gut microbiota promotes macrophage M1 polarization in hepatic sinusoidal obstruction syndrome via regulating intestinal barrier function mediated by butyrate

https://www.tandfonline.com/doi/full/10.1080/19490976.2024.2377567

DOI:https://doi.org/10.1080/19490976.2024.2377567

Hepatic sinusoidal obstruction syndrome (HSOS) is a rare disease targeting hepatic sinusoids, sublobular veins, and central veins of the liver lobules. This article primarily discusses the role of gut microbiota and macrophage activation in the progression of HSOS induced by pyrrolizidine alkaloids. Researchers induced an HSOS mouse model using monocrotaline (MCT) via forced feeding. They then analyzed the fecal microbiota composition using 16S ribosomal DNA sequencing. The study found that depletion of macrophages in the mouse model alleviated inflammation and apoptosis in the liver. Fecal butyrate levels were significantly reduced in HSOS mice, and butyrate supplementation partially mitigated liver damage and improved both in vitro and in vivo gut barrier function. Additionally, increased levels of portal vein lipopolysaccharides and a higher proportion of M1 macrophages in the liver were detected in HSOS-FMT mice and untreated mice. For more detailed information, please refer to the original article.

3.Gut proinflammatory bacteria is associated with abnormal functional connectivity of hippocampus in unmedicated patients with major depressive disorder

https://www.nature.com/articles/s41398-024-03012-9

DOI: 10.1038/s41398-024-03012-9

Major depressive disorder (MDD) is a severe chronic mental illness. Research has found that dysbiosis of gut bacteria in MDD is associated with changes in the function and structure of the hippocampus in the brain. This study included a total of 44 unmedicated MDD patients and 42 healthy controls. By comparing magnetic resonance imaging (MRI) data and fecal sample data, it was found that MDD patients exhibited increased functional connectivity between the left and right hippocampus. However, functional connectivity between the right hippocampal CA3 region and bilateral posterior cingulate cortex was decreased. Additionally, the analysis of fecal bacteria revealed an increase in the levels of Firmicutes and a decrease in the levels of bacteria that produce short-chain fatty acids (SCFAs) in MDD patients. There was a positive correlation between the functional connectivity values of the left hippocampal CA3-right hippocampal (CA2 and CA3) and the relative abundance of Enterobacteriaceae in MDD patients. These findings may shed light on the potential role of gut microbiota in the neuropathology of MDD. For more detailed information, please refer to the original article.

4.The Role of Gut Microbiota in the Neuroprotective Effects of Selenium in Alzheimer's Disease

https://link.springer.com/article/10.1007/s12035-024-04343-w

DOI:10.1007/s12035-024-04343-w

Previous studies have found that supplementation with selenium in cell and animal models of Alzheimer's disease can reduce the formation of amyloid-beta (Aβ) plaques and tau phosphorylation. Selenium also reverses the decline in brain antioxidant levels, inhibits neuronal oxidative stress and the production of pro-inflammatory cytokines, and improves synaptic plasticity and neurogenesis, collectively enhancing cognitive function. Recent research has suggested that the neuroprotective effects of selenium may be related to its regulation of gut microbiota. Supplementation with selenium has been shown to improve the biodiversity of gut microbiota, increasing the relative abundance of Lactobacillus, Bifidobacterium, and Desulfovibrio, while decreasing the relative abundance of Lachnospiraceae_NK4A136, Rikenella, and Helicobacter. For more detailed information on selenium and Alzheimer's disease, please refer to the review article.

5.Gut microbial factors predict disease severity in a mouse model of multiple sclerosis

https://www.nature.com/articles/s41564-024-01761-3

DOI: 10.1038/s41564-024-01761-3

The relationship between gut bacteria and neurodegenerative diseases is recognized, but other risk factors beyond microbiome composition are limited. This article utilizes preclinical models of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) to identify microbial risk factors. By analyzing six combinations of different genotypes and complex microbiomes or human microbiomes in mice, the study examines the likelihood of severe neuroinflammation occurring. The article emphasizes that when predicting the severity of neuroinflammation, it is crucial to consider the bidirectional interactions between microbial community networks and host specificity. For more detailed information, please refer to the original article.