This chapter systematically elucidates the biological mechanisms of inflammation and its pathological consequences, with an in-depth analysis of the anti-inflammatory effects and molecular pathways of tea bioactive compounds. Inflammation, as a core defense response to injury, is triggered by multiple factors including microbial infections, physicochemical stimuli, and immune dysregulation. The process involves vascular activation, immune cell infiltration, and release of inflammatory mediators, regulated by transcription factors such as NF-κB/AP-1. Chronic inflammation contributes to tissue fibrosis and is closely associated with multiple diseases (e.g., IBD, liver disease, brain dysfunction). Studies demonstrate that tea components—notably polyphenols, theanine, polysaccharides, and theaflavins—exert synergistic anti-inflammatory effects through multiple pathways: Direct actions: Suppressing COX-2/iNOS activity to reduce PGE2/NO production and inflammatory mediator secretion. Signaling modulation: Inhibiting IKK/IκB phosphorylation to block NF-κB nuclear translocation, downregulating MAPK pathway activation, and balancing AKT/JNK signaling. Immunoregulation: Promoting macrophage polarization toward the M2 phenotype, modulating Treg/Th17 ratios, and enhancing gut barrier function. Microecological remodeling: Reshaping gut/oral microbiota, promoting SCFA and bile acid metabolism. In disease applications, tea components ameliorate colonic injury in IBD, hepatic steatosis in alcoholic liver disease, and depression-like behaviors via the gut-liver/brain axis, while inhibiting pathogenic biofilm formation and periodontal inflammation in oral disorders.