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The gut microbiota plays a critical role in maintaining human health, influencing a wide range of physiological processes, including immune regulation, metabolism, and neurological function. Recent studies have shown that imbalances in gut microbiota composition can contribute to the onset and progression of various diseases, such as metabolic disorders (e.g., obesity and diabetes) and neurodegenerative conditions (e.g., Alzheimer's and Parkinson's). These conditions are often accompanied by chronic inflammation and dysregulated immune responses, which are closely linked to specific forms of cell death, including pyroptosis and ferroptosis. Pathogenic bacteria in the gut can trigger these cell death pathways through toxin release, while probiotics have been found to mitigate these effects by modulating immune responses. Despite these insights, the precise mechanisms through which the gut microbiota influences these diseases remain insufficiently understood. This review consolidates recent findings on the impact of gut microbiota in these immune‐mediated and inflammation‐associated conditions. It also identifies gaps in current research and explores the potential of advanced technologies, such as organ‐on‐chip models and the microbiome–gut–organ axis, for deepening our understanding. Emerging tools, including single‐bacterium omics and spatial metabolomics, are discussed for their promise in elucidating the microbiota's role in disease development.
The gut microbiota plays a critical role in maintaining human health, influencing a wide range of physiological processes, including immune regulation, metabolism, and neurological function. Recent studies have shown that imbalances in gut microbiota composition can contribute to the onset and progression of various diseases, such as metabolic disorders (e.g., obesity and diabetes) and neurodegenerative conditions (e.g., Alzheimer's and Parkinson's). These conditions are often accompanied by chronic inflammation and dysregulated immune responses, which are closely linked to specific forms of cell death, including pyroptosis and ferroptosis. Pathogenic bacteria in the gut can trigger these cell death pathways through toxin release, while probiotics have been found to mitigate these effects by modulating immune responses. Despite these insights, the precise mechanisms through which the gut microbiota influences these diseases remain insufficiently understood. This review consolidates recent findings on the impact of gut microbiota in these immune‐mediated and inflammation‐associated conditions. It also identifies gaps in current research and explores the potential of advanced technologies, such as organ‐on‐chip models and the microbiome–gut–organ axis, for deepening our understanding. Emerging tools, including single‐bacterium omics and spatial metabolomics, are discussed for their promise in elucidating the microbiota's role in disease development.
BACKGROUND Alcoholic liver disease (ALD) is a common liver disease caused by long-term alcohol consumption, the specific molecular mechanism of which is still unclear. It may be influenced to some extent by ferroptosis and P.g, which is an important pathogen of periodontitis. MARERIALS AND METHODS: C57BL/6 mice and AML12 cells were selected as study subjects. The periodontitis model was induced by P.g and the alcoholic liver model was created. Pathological analysis was performed on liver, intestine and periodontal, and 16S rRNA was to analyze changes in intestinal flora and intestinal gap junction protein (ZO1, Occludin) levels in each group. Ferroptosis indices were detected in the liver tissues and AML12. RESULTS Oral exposure to P.g can induce mice periodontitis and exacerbate alcohol-related liver injury. Both alcohol and P.g can cause intestinal flora disturbance, damage to the intestinal epithelial barrier, increased permeability and activation of mouse hepatocyte ferroptosis, and P.g can aggravate such alcohol-induced liver damage. CONCLUSION Both alcohol and P.g can cause intestinal flora disturbance, damage to the intestinal epithelial barrier, increased permeability and activation of mouse hepatocyte ferroptosis, and P.g can aggravate such alcohol-induced liver damage. ACSL4 and HO-1 play the important role in exacerbation of alcoholic liver injury by P.g.
Objective Porphyromonas gingivalis ( P. gingivalis ) is considered the predominant pathogen in association with different stages of periodontitis, and fim genes play a vital role in adherence and colonization. This study is thus aimed to detect the prevalence of P. gingivalis and the frequency of fim gene types among the clinical strains isolated from periodontitis patients. Methods Plaque samples (N = 45) were collected from patients with three different stages of periodontitis (n = 15 in each group). All the samples were inoculated onto sterile anaerobic blood agar and were processed anaerobically using a GasPak system at 37°C for five to seven days. Standard microbiological techniques were used to identify P. gingivalis . Genomic DNA was extracted, and polymerase chain reaction (PCR) was carried out to detect the frequency of three fim gene types, using specific primers. Results P. gingivalis was more prevalent in Group III (93.3%), followed by 26.7% in Group II, and 13.3% in Group I. Maximum isolates were seen in the age group of 40-50, with no significance within the genders. fim type I was frequent in Group III (78.5% (n = 11)), followed by 0.25% (n = 1) under Group II, with no other fim types in the other groups. Conclusion Prevalence of P. gingivalis and frequency of fim genes, in association with its virulence, were observed. Periodical monitoring of such virulence genes would aid in the theranostic approach to combat the complications caused by P. gingivalis in periodontitis cases.
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