ObjectiveSepsis is the leading cause of death in critically ill patients. The gastrointestinal tract has long been thought to play an important role in the pathophysiology of sepsis. Antibiotic therapy can reduce a patient’s commensal bacterial population and raise their risk of developing subsequent illnesses, where gut microbiota dysbiosis may be a key factor.MethodsIn this study, we analyzed the 16S rRNA of fecal samples from both healthy people and patients with sepsis to determine if alterations in gut bacteria are associated with sepsis. Then, we developed a mouse model of sepsis using cecal ligation and puncture (CLP) in order to examine the effects of fecal microbiota transplantation (FMT) and short-chain fatty acids (SCFAs) on survival rate, systemic inflammatory response, gut microbiota, and mucosal barrier function.ResultsSepsis patients’ gut microbiota composition significantly differed from that of healthy people. At the phylum level, the amount of Proteobacteria in the intestinal flora of sepsis patients was much larger than that of the control group, whereas the number of Firmicutes was significantly lower. Mice with gut microbiota disorders (ANC group) were found to have an elevated risk of death, inflammation, and organ failure as compared to CLP mice. However, all of these could be reversed by FMT and SCFAs. FMT and SCFAs could regulate the abundance of bacteria such as Firmicutes, Proteobacteria, Escherichia Shigella, and Lactobacillus, restoring them to levels comparable to those of healthy mice. In addition, they increased the expression of the Occludin protein in the colon of mice with sepsis, downregulated the expression of the NLRP3 and GSDMD-N proteins, and reduced the release of the inflammatory factors IL-1β and IL-18 to inhibit cell pyroptosis, ultimately playing a protective role in sepsis.DisccusionFMT and SCFAs provide a microbe-related survival benefit in a mouse model of sepsis, suggesting that they may be a viable treatment for sepsis.

Purpose Gasdermin D (GSDMD) is a cytoplasmic protein that is encoded by the gasdermin family GSDMD gene and is the ultimate executor of pyroptosis. Pyroptosis is a mode of lysis and inflammation that regulates cell death, ultimately leading to cell swelling and rupture. In sepsis, a dysregulated host response to infection frequently results in hyperinflammatory responses and immunosuppression, eventually leading to multiple organ dysfunction. Pyroptosis regulates innate immune defenses and plays an important role in the process of inflammatory cell death, and the absence of any link in the entire pathway from GSDMD to pyroptosis causes bacterial clearance to be hampered. Under normal conditions, the process of pyroptosis occurs much faster than apoptosis, and the threat to the body is also much greater. Materials and methods We conducted a systematic review of relevant reviews and experimental articles using the keywords sepsis, Gasdermin D, and Pyroptosis in the PubMed, Scopus, Google Scholar, and Web of Science databases. Conclusion Combined with the pathogenesis of sepsis, it is not difficult to find that pyroptosis plays a key role in bacterial inflammation and sepsis. Therefore, GSDMD inhibitors may be used as targeted drugs to treat sepsis by reducing the occurrence of pyroptosis. This review mainly discusses the key role of GSDMD in sepsis.

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BackgroundWild edible mushrooms are rich in nutrition and popular with people; however, few laboratory studies are available about the predictability of outcomes among patients with mushroom poisoning. Therefore, this study aimed to analyze the clinical features and death risk factors of patients with mushroom poisoning.MethodsPatients with mushroom poisoning admitted to the hospital from 2015 to 2021 were retrospectively evaluated.ResultsA total of 197 patients with mushroom poisoning were enrolled in this study, of which 100 (50.76%) were males, and the mortality was 10.66% (21/197). Patients who died were more likely to have demonstrated a long latency, high alanine aminotransferase, aspartate aminotransferase, direct bilirubin, total bilirubin (TB), activated partial thromboplastin time, prothrombin time, international normalized ratio, creatinine, and blood urea nitrogen. Multiple logistic regression analysis indicated that TB level greater than or equal to 34.2 μmol/L had the greatest lethal risk and could increase the risk of death by 14.588 times (odds ratio: 15.588; 95% confidence interval: 2.088–116.351), which indicated that TB was an independent risk factor of death in patients with acute mushroom poisoning.ConclusionBilirubin concentration was associated with the increased likelihood of mortality. Total bilirubin was the independent risk factor of mushroom poisoning.