Microbiota–host crosstalk in ulcerative colitis: mechanistic evidence and translational prospects for traditional Chinese medicine

Ulcerative colitis (UC) is sustained by reciprocal interactions among intestinal dysbiosis, altered microbial metabolism, epithelial barrier dysfunction, and mucosal immune activation. This narrative review examines that microbiota–metabolism–barrier–immune network and evaluates how traditional Chinese medicine (TCM) may influence it. Human multi-omics studies indicate that UC-associated dysbiosis is more reproducible at the level of microbial function and metabolite output than at the level of individual taxa. Experimental studies further implicate short-chain fatty acids, bile acids, tryptophan-derived indoles, arginine, and choline-related metabolites in epithelial and immune regulation. Most evidence for TCM-mediated microbiota modulation, however, comes from chemically induced experimental colitis, organoid, or cell systems; human interventional evidence remains limited. We therefore grade mechanistic evidence from association through microbiota dependence, candidate strain/metabolite sufficiency, host-target validation, and integrated causal-chain validation. This distinction avoids treating genus-level relative-abundance changes as proof of microbial benefit or mediation. Emerging clinical trials of indigo naturalis, Curcumin–QingDai, Andrographis paniculata extract, curcumin, and selected multicomponent Chinese herbal therapies provide short-term efficacy signals, but results are preparation- and dose-dependent and do not yet establish microbiota-mediated clinical efficacy. Translation will require chemically standardized products, rigorous safety surveillance, strain- and function-resolved microbiome measurements, explicit experiments separating direct herbal actions from microbiota-dependent effects, and clinical trials incorporating endoscopic, histological, pharmacokinetic, microbial, metabolic, and long-term safety outcomes.