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. 2018 Oct 25;316(2):L334–L347. doi: 10.1152/ajplung.00206.2018

Fig. 9.

Fig. 9.

Proposed mechanism for myeloid differentiation factor 88 (MyD88) control of mucin (Muc)5ac responses in the airway epithelium during broad Toll-like receptor (TLR) activation from organic dust extract (ODE). A: ODE consists of gram-positive and -negative bacterial cell-wall components that induce innate-immune pathways through the parallel activation of TLR-MyD88 leading to neutrophil recruitment and second, a modest mucus production leading to enhanced mucociliary clearance. MyD88 signaling dampens mucin production in favor of neutrophil chemotaxis following ODE-mediated inflammation. B: in MyD88-deficient airway epithelium, mucus production is enhanced to compensate for lack of an inflammatory response. Thin arrows, modest activation; thick arrows, significant activation; X, MyD88-KO; →, transcriptional regulation.