Clustered regularly interspaced short palindromic repeats (CRISPR) and their CRISPR-associated proteins (Cas) are an adaptive immune system involved in specific defenses against the invasion of foreign mobile genetic elements, such as plasmids and phages. This study aims to analyze the gene structure and to explore the function of the CRISPR system in the Enterococcus genome, especially with regard to drug resistance. The whole genome information of 110 enterococci was downloaded from the NCBI database to analyze the distribution and the structure of the CRISPR-Cas system including the Cas gene, repeat sequences, and spacer sequence of the CRISPR-Cas system by bioinformatics methods, and to find drug resistance-related genes and analyze the relationship between them and the CRISPR-Cas system. Multilocus sequence typing (MLST) of enterococci was performed against the reference MLST database. Information on the drug resistance of Enterococcus was retrieved from the CARD database, and its relationship to the presence or absence of CRISPR was statistically analyzed. Among the 110 Enterococcus strains, 39 strains (35.45%) contained a complete CRISPR-Cas system, 87 CRISPR arrays were identified, and 62 strains contained Cas gene clusters. The CRISPR system in the Enterococcus genome was mainly type II-A (59.68%), followed by type II-C (33.87%). The phylogenetic analysis of the cas1 gene sequence was basically consistent with the typing of the CRISPR-Cas system. Of the 74 strains included in the study for MLST typing, only 19 (25.68%) were related to CRISPR-Cas typing, while the majority of the strains (74.32%) of MLST typing were associated with the untyped CRISPR system. Additionally, the CRISPR-Cas system may only be related to the carrying rate of some drug-resistant genes and the drug-resistant phenotype. In conclusion, the distribution of the enterococcus CRISPR-Cas system varies greatly among different species and the presence of CRISPR loci reduces the horizontal transfer of some drug resistance genes.

Transfer RNA-derived small RNAs (tsRNAs) are a newly discovered class of small noncoding RNAs (sncRNAs) that include tRNA-derived stress-induced RNAs (tiRNAs) and tRNA-derived fragments (tRFs). Following the development of high-throughput sequencing technology, an increasing number of tsRNAs have been discovered with vital functions in different physiological and pathophysiological processes. Extensive research has revealed that tsRNAs are involved in various diseases, such as cancers, autoimmune illnesses and other diseases. This review focuses on the role and significance of tsRNAs in inflammation, such as the regulation of substances including inflammatory inducers, inflammatory cells and inflammatory factors, which contribute to the pathogenesis of inflammation-related diseases. Moreover, we discuss in-depth the molecular pathogenic mechanisms of tsRNAs in inflammation-related diseases through different signaling pathways and assess their clinical value, providing new perspectives for the exploration of tsRNA functions and inflammation-related diseases.

Background Crohn’s disease (CD) is a chronic, nonspecific inflammatory bowel disease with a poor prognosis. Despite its increasing incidence, curing CD remains challenging due to its complex etiology and unclear pathogenesis. Methods A comprehensive PubMed and Web of Science search was conducted using the keywords Crohn’s disease, gut microbiota, dysbiosis, pathogenesis and treatment, focusing on studies published between 2014 and 2024. Results Recent studies have demonstrated a close relationship between gut microbiota dysbiosis and the development of CD. Although many dysbioses associated with CD have not yet been proven to be causal or consequential, it has been observed that the gut microbiota in CD patients exhibits reduced diversity, a decrease in beneficial bacteria, and an increase in pathogenic bacteria. These changes may lead to decreased intestinal barrier function, abnormal immune responses, and enhanced inflammatory reactions, which are related to the disease’s activity, phenotype, drug treatment efficacy, and postoperative therapeutic outcomes. Therefore, further exploration of the microbiota-host interactions and the pathogenesis of CD, the identification of biomarkers, and the development of targeted strategies for modulating the gut microbiota could offer new avenues for the prevention and treatment of CD. Conclusions This review highlights the pivotal role of gut microbiota dysbiosis in driving CD pathogenesis and its progression, while underscoring its potential as a therapeutic target through dietary modulation, microbial interventions, and integrative strategies to improve clinical management and prognostic outcomes.

The rising incidence of Crohn’s disease (CD) in Asia underscores the need to explore its underlying mechanisms. The interaction between gut microbiota and the host is strongly linked to CD onset and progression, yet the precise mechanisms remain unclear. Previous studies have demonstrated that Ruminococcus gnavus (R. gnavus) is closely associated with the development and progression of CD. Therefore, this study focuses on the inflammatory role of R. gnavus in CD pathogenesis. We performed comprehensive 16 S rRNA sequencing on fecal samples from active CD patients, inactive CD patients, and healthy controls. Alongside this, we conducted clinical data and correlation analyses. To identify key microbial genera, we developed and validated a random forest classification model. Additionally, we utilized a dextran sulfate sodium (DSS)-induced colitis model in C57BL/6 mice to explore the inflammatory role of R. gnavus (ATCC 29149). Our analysis revealed significant shifts in gut microbiome composition across different stages of CD compared to healthy controls. Notably, there was a marked decrease in Agathobacter and an increase in R. gnavus in patients with active CD. The random forest classification model, which was based on six specific genera (Agathobacter, Vicinamibacteraceae, Arthrobacter, Eubacterium coprostanoligenes group, Ruminococcus gnavus group, and Prevotella 9), achieved an AUC of 0.912, effectively distinguishing CD patients from healthy controls. In the DSS-induced colitis model, R. gnavus exacerbated inflammation, significantly increasing levels of IL-6 and TNF-α, and significantly decreasing levels of Claudin-1 and MUC2, further underscoring its critical role in CD pathogenesis. The identified genera demonstrate potential as diagnostic biomarkers for CD, with R. gnavus playing a key role in the disease’s pathogenesis by inducing inflammation in colitis models.

Purpose: Ulcerative colitis (UC) is an inflammatory bowel disease with an unclear etiology that can lead to irreversible changes in distal colonic function in chronic patients. This study investigated anorectal function in recurrent UC patients and identified influencing factors. Methods: This prospective study enrolled 33 recurrent UC patients and 40 newly diagnosed patients from January 2019 to December 2022. Data collection included clinical records, scores, and anorectal function assessments. Regression analyses were used to identify factors impacting anorectal function. Results: Recurrent UC patients had higher baseline CRP and fecal calprotectin levels, increased anxiety and depression, and more severe fecal incontinence. They also had lower BMIs, serum Hb and albumin (ALB) levels, and Inflammatory Bowel Disease Questionnaire scores than did initial-onset UC patients. Multivariate linear regression analysis revealed that long disease duration (coef. − 0.376, P < 0.001) and high fecal calprotectin level (coef. − 0.656, P < 0.001) independently influenced the initial sensation threshold in recurrent UC patients. Additionally, high fecal calprotectin (coef. − 0.073, P = 0.013) and high Zung Self-Rating Anxiety Scale score (coef. − 0.489, P = 0.001) were identified as two independent determinants of the defecation volume threshold. For the defecation urgency threshold, the independent factors included high disease duration (coef. − 0.358, P = 0.017) and high fecal calprotectin level (coef. − 0.499, P = 0.001). Similarly, the sole independent factor identified for the maximum capacity threshold was high fecal calprotectin (coef. − 0.691, P = 0.001). Conclusion: Recurrent UC patients had increased rectal sensitivity and compromised anorectal function, which significantly impacted quality of life. Proactively managing the disease, reducing UC relapses, and addressing anxiety are effective measures for improving anorectal function in these patients.