FIG 2.

Potential mechanisms for microbiota-regulated processes in CRS. A, Commensal bacteria are niche occupiers precluding colonization or overgrowth of potential pathogens. This can occur directly through the production of bacteriocins, or it may occur indirectly by competition for local resources or induction of various antimicrobial peptides from the apical epithelium. B, Commensal organisms are critical for immune maturation, as has been documented in mouse gut and upper airway studies. Gain of pathogens may direct proinflammatory imbalance over anti-inflammatory homeostatic immune activities. C, Commensal organisms may provide several metabolic actions in the complex apical surface milieu, including biosynthesis of important proteins, degradation of airborne or locally produced toxins to innocuous byproducts, and digestion of mucins into energy sources such as short chain fatty acids. D, Breakdown of the epithelial barrier is a hallmark of CRS, with translocation of microbes into the subepithelial compartment. This can propagate the proinflammatory state. PRR, Pathogen recognition; Treg, regulatory T.