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The gut microbiota-host immune-inflammatory axis is a complex bidirectional communication network between the intestinal microbial community and the host's immune system [1]. This axis plays a critical role in maintaining physiological homeostasis by training the immune system to distinguish between commensal organisms and pathogens, largely through the production of microbial metabolites like short-chain fatty acids (SCFAs) [2][3]. Dysbiosis, or an imbalance in this microbial ecosystem, is linked to various inflammatory and autoimmune conditions, including inflammatory bowel disease (IBD), metabolic syndrome, and neuroinflammation [4]. Microbial therapies, such as fecal microbiota transplantation (FMT), probiotics, and defined bacterial consortia, aim to indirectly modulate host inflammatory pathways by restoring microbial diversity and promoting anti-inflammatory signaling [5]. These interventions work by outcompeting pathogens, strengthening the intestinal epithelial barrier, and inducing the differentiation of regulatory T cells (Tregs) [6]. As a therapeutic strategy, targeting this axis offers a novel approach to treating systemic inflammation by addressing the microbial triggers of immune dysregulation.
Indirect modulation of host immune signaling via microbial metabolites (e.g., SCFAs acting on GPR41/43), competitive inhibition of pathogens, restoration of epithelial barrier integrity, and activation of pattern recognition receptors (PRRs) to promote immune tolerance.
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