Evidence for diminished levels of epithelial psoriasin and calprotectin in chronic rhinosinusitis

Background: Decreased epithelial expression of mRNA for S100A7 (psoriasin) and S100A8/A9 (calprotectin) has been reported in patients with chronic rhinosinusitis (CRS). Objectives: We sought to assess whether the expression of S100 proteins is also altered in the sinonasal cavity of patients with CRS. Methods: We determined levels of S100 proteins in nasal lavage fluid and sinonasal tissue extracts from patients with CRS using ELISA and immunohistochemical analysis of nasal polyp tissue from patients with CRS with nasal polyps and uncinate tissue from healthy control subjects, patients with CRSsNP, and patients with CRSwNP. Results: Expression levels of S100 proteins were decreased compared with those seen in control subjects in nasal lavage fluid from both CRS groups (P < .05). Similarly, tissue expression of these proteins assessed by means of immunohistochemistry demonstrated clear reductions, primarily in the epithelial lining. Interestingly, levels of calprotectin were increased in nasal polyp tissue despite lower levels in lavage fluid. Levels of calprotectin in nasal tissues were correlated with levels of neutrophils, as assessed by means of quantification of neutrophil elastase. Conclusions: Several S100 proteins are in the epidermal differentiation complex of genes and have been demonstrated to play a role in maintenance of barrier function and formation of an antimicrobial shield. We demonstrate significantly decreased levels of expression of S100 proteins in the epithelium of patients with CRS, which might lead to diminished innate immune responses and barrier function. Increased levels of calprotectin in nasal polyp tissue might reflect neutrophil recruitment and a compensatory mechanism. Future studies will he important to determine whether reduced levels of S100 proteins lead to decreased antimicrobial responses in the upper airways and sinuses and whether this reduction plays a causative role in CRS pathogenesis and susceptibility to infectious disease. (J Allergy Clin Immunol 2010;125:667-75.)