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.

Introduction: Calcium oxalate (CaOx) nephrolithiasis is a major global health burden with limited non-pharmacological preventive options. Although moderate beer consumption has been linked to a lower risk of stone formation, the underlying mechanisms remain unclear. This study aimed to investigate the anti-lithogenic effects of dietary beer and the molecular pathways involved. Methods: We combined a retrospective clinical analysis of 415 urolithiasis patients with a glyoxylic acid–induced mouse model. Male C57BL/6J mice received low-/high-dose beer (3/6 mL/kg) by gavage. We assessed renal histology, urinary biochemistry, oxidative stress, inflammatory responses, and the expression of crystal-adhesion molecules (CD44, OPN, Kim-1). Results: In the clinical cohort, calcium oxalate monohydrate (COM) stones predominated (79.0%), with a male predominance (2.1:1). In mice, beer intervention lowered urinary oxalate and calcium concentrations, reduced histopathological injury and collagen deposition, downregulated CD44/OPN protein, decreased CD44/Kim-1/TNF-α/IL-1β mRNA expression, and partially preserved catalase and superoxide dismutase activities. The benefits were unlikely attributable to ethanol-induced diuresis, given the minimal gavage volume (~1.2–4% of fluid intake) and low ethanol delivery (~1.4–2.8 mg), which was further supported by unchanged daily water consumption. Discussion: These findings demonstrate that dietary beer attenuates CaOx stone formation and modulates urinary, inflammatory, oxidative, and adhesion markers. The anti-lithogenic potential of beer constituents supports the development of purine-free, non-alcoholic, hops-derived polyphenol preparations as a testable hypothesis. However, the absence of appropriate controls precludes attributing the effects to any single component, and these results should not be interpreted as a clinical recommendation to consume beer.