Research on the microbiome is reshaping the conceptual foundations of inflammatory diseases. As a dynamic component of the host ecosystem, microbial communities collectively influence inflammatory responses and homeostatic balance through their metabolites, structural signals, and interactions with immune pathways. Dysbiosis can amplify immune activation and metabolic disturbances, leading to persistent inflammation, whereas specific commensal taxa and their metabolites possess the capacity to suppress excessive immune responses and restore homeostasis. This bidirectional regulatory capacity positions the microbiome as a central node that both drives and modulates inflammatory networks. Multi-omics investigations have delineated the systemic architecture of microbe-host interactions, revealing cross-system axes such as the gut-brain, gut-liver, and skin-gut pathways that constitute a signaling framework integrating inflammation and immunity, thereby reshaping our understanding of disease pathogenesis. Within this framework, inflammation is redefined as an adaptive strategy for maintaining systemic stability rather than merely a singular pathological reaction. Therapeutic approaches including fecal microbiota transplantation (FMT), engineered microbial strains, and interventions targeting metabolic signaling are propelling microecological medicine into an era of precision modulation. As systems biology converges with spatial omics, research on the microbiome is shifting from descriptive pathology toward mechanistic control, establishing it as a critical nexus linking immunity, metabolism, and disease evolution. This transformation heralds a paradigm shift in medicine from merely "suppressing inflammation" to actively "reconstructing ecological order."
Liao et al. (2026) studied this question.