Fig. 1

Schematic representation of CRS tissue. A proposed model for the changes of the sinonasal environment during CRS. Increased mucus production and/or goblet cell hyperplasia can result in a mucus layer with increased thickness (I). Changes in sinus microbiota can be observed, more specifically the abundances of CRS-associated pathogens S. aureus, P. aeruginosa, S. pneumoniae and H. influenza. Proposed changes involve decreased epithelial integrity (III: defective epithelial barrier function), with increased glucose concentrations in the airway surface liquid (II), decreased recognition of acyl-homoserine lactones by T2R38 receptors, altered cytokine production and decreased antimicrobial protein and immunoglobulin production that occur in CRS compared to healthy tissue. These changes potentially provide an environment that promotes pathogenic bacterial growth and invasion of the epithelial barrier (IV), resulting in chronic inflammation. S. aureus has the ability to produce a super-antigen, which evades conventional immune response and directly elicits eosinophilia and a T _H 2-skewed immune response (IL-5, IL-13, IL-4), whereas IFN-γ induces a T _H 1-skewed immune response (figure adapted from Mahdavinia et al. [40])