Bile acids (BAs) play a crucial role in the human body’s defense against infections caused by bacteria, fungi, and viruses. BAs counteract infections not only through interactions with intestinal bacteria exhibiting bile salt hydrolase (BSH) activity but they also directly combat infections. Building upon our research group’s previous discoveries highlighting the role of BAs in combating infections, we have initiated an in-depth investigation into the interactions between BAs and intestinal microbiota. Leveraging the existing literature, we offer a comprehensive analysis of the relationships between BAs and 16 key microbiota. This investigation encompasses bacteria (e.g., Clostridioides difficile (C. difficile), Staphylococcus aureus (S. aureus), Escherichia coli, Enterococcus, Pseudomonas aeruginosa, Mycobacterium tuberculosis (M. tuberculosis), Bacteroides, Clostridium scindens (C. scindens), Streptococcus thermophilus, Clostridium butyricum (C. butyricum), and lactic acid bacteria), fungi (e.g., Candida albicans (C. albicans) and Saccharomyces boulardii), and viruses (e.g., coronavirus SARS-CoV-2, influenza virus, and norovirus). Our research found that Bacteroides, C. scindens, Streptococcus thermophilus, Saccharomyces boulardii, C. butyricum, and lactic acid bacteria can regulate the metabolism and function of BSHs and 7α-dehydroxylase. BSHs and 7α-dehydroxylase play crucial roles in the conversion of primary bile acid (PBA) to secondary bile acid (SBA). It is important to note that PBAs generally promote infections, while SBAs often exhibit distinct anti-infection roles. In the antimicrobial action of BAs, SBAs demonstrate antagonistic properties against a wide range of microbiota, with the exception of norovirus. Given the intricate interplay between BAs and intestinal microbiota, and their regulatory effects on infections, we assert that BAs hold significant potential as a novel approach for preventing and treating microbial infections.

Human health is influenced by the gut microbiota, particularly in aspects of host immune homeostasis and intestinal immune response. Tryptophan (Trp) not only acts as a nutrient enhancer but also plays a critical role in the balance between host immune tolerance and gut microbiota maintenance. Both endogenous and bacterial metabolites of Trp, exert significant effects on gut microbial composition, microbial metabolism, the host immunity and the host-microbiome interface. Trp metabolites regulate host immunity by activating aryl hydrocarbon receptor (AhR), thereby contributing to immune homeostasis. Among Trp metabolites, AhR ligands include endogenous metabolites (such as kynurenine), and bacterial metabolites (such as indole and its derivatives). Here, we present a comprehensive analysis of the relationships between Trp metabolism and 14 key microbiota, encompassing fungi (e.g., Candida albicans, Aspergillus), bacteria (e.g., Ruminococcus gnavus, Bacteroides, Prevotella copri, Clostridium difficile, Escherichia coli, lactobacilli, Mycobacterium tuberculosis, Pseudomonas aeruginosa, Staphylococcus aureus, Helicobacter. Pylori), and viruses (e.g., SARS-CoV-2, influenza virus). This review clarifies how the gut microbiota regulates Trp metabolism and uncovers the underlying mechanisms of these interactions. And increased mechanistic insight into how the microbiota modulate the host immune system through Trp metabolism may allow for the identification of innovative therapies that are specifically designed to target Trp absorption, Trp metabolites, the gut microbiota, or interactions between Trp and gut microbiota to treat both intestinal and extra-intestinal inflammation as well as microbial infections.

Background: Sepsis is a dysregulated host response to pathogens. Delay in sepsis diagnosis has become a primary cause of patient death. This study determines some factors to prevent septic shock in its early stage, contributing to the early treatment of sepsis. Methods: The sequencing data (RNA- and miRNA-sequencing) of patients with septic shock were obtained from the NCBI GEO database. After re-annotation, we obtained lncRNAs, miRNA, and mRNA information. Then, we evaluated the immune characteristics of the sample based on the ssGSEA algorithm. We used the WGCNA algorithm to obtain genes significantly related to immunity and screen for important related factors by constructing a ceRNA regulatory network. Result: After re-annotation, we obtained 1708 lncRNAs, 129 miRNAs, and 17 326 mRNAs. Also, through the ssGSEA algorithm, we obtained 5 important immune cells. Finally, we constructed a ceRNA regulation network associated with SS pathways. Conclusion: We identified 5 immune cells with significant changes in the early stage of septic shock. We also constructed a ceRNA network, which will help us explore the pathogenesis of septic shock.