Figure 1. Upper-airway dysbiosis and potential immunopathology in the airway inflammation. Persistent exposure to pathogens and other risk factors promotes airway inflammation through induction of both innate immune cells and adaptive immune cells. Although some risk factors are prominently related to upper airway dysbiosis, host factors are also considerably overlap in the development of airway diseases. Mucins in interaction with IgA and AMP contribute to innate immunity. Upon microbial signals, DCs activate antigen-specific naïve T cells which further drive development in effector Th cells. Tregs can suppress various effector Th cell subsets releasing anti-inflammatory and immunoregulatory cytokines, yet are downregulated in chronic airway inflammation. Th2 derived cytokine IL-13 upregulates the expression of mucin genes that initiate mucus hypersecretion. Pathogen invasion also induces epithelium-derived IL-6 and IL-8 production via interaction with PRR leading to neutrophilic inflammation.