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It also altered immune mediatorsupregulating Cxcl2 and Il-6 while suppressing Ifn- and Tgf- thereby disturbing mucosal homeostasis through concurrent shifts in microbiota, mucus composition, and cytokine signaling (Fig

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-CBT-diol inhibited the viability of five prostate cancer cell lines PC-3MPC-3CWR-R1caDU-145 and CWR-22rv1, reduced their migration and colony formation

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These microbial and transcriptomic changes exacerbated inflammatory injury in early COPD, as corroborated in murine models, highlighting the interplay between smoking, airway microbiota, and disease pathogenesis [15]

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