Reduced Expression of Antimicrobial Palate, Lung and Nasal Epithelial Clone (PLUNC) protein in Polyps from Patients with Chronic Rhinosinusitis is Due to Decreased Number of Glands

S U N D A Y 531 Elevated Expression of CC Chemokine Ligand 18 in Chronic Rhinosinusitis A. Kato, S. Peterson, J. A. Poposki, D. R. Nagarkar, R. T. Chustz, A. T. Peters, L. A. Suh, R. Carter, J. Norton, K. E. Harris, L. C. Grammer, B. Tan, R. K. Chandra, D. B. Conley, R. C. Kern, R. P. Schleimer; Division of Allergy-Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL, Department of Otolaryngology, Northwestern University Feinberg School of Medicine, Chicago, IL. RATIONALE: Chronic rhinosinusitis with nasal polyps (CRSwNP) is associated with Th2-dominant inflammation including eosinophilia, in contrast to non-polypoid CRS (CRSsNP). CCL18/PARC is a CC chemokine known to recruit na€ive T cells, B cells, and immature dendritic cells, and thought to be involved in Th2-related inflammatory diseases including asthma and atopic dermatitis. However, expression of CCL18 in CRS has not been extensively studied. METHODS:Using nasal polyp tissue (NP) and uncinate tissue (UT) from controls and patients with CRS, we examined the expression of CCL18 mRNA by real-time PCR and assayed CCL18 protein by ELISA, immunohistochemistry and western blot. RESULTS: Compared to control subjects (n59), CCL18 mRNAwas significantly increased in NP (432-fold, p<0.001, n526) and UT (109-fold, p50.009, n519) from patients with CRSwNP but not in UT from patients with CRSsNP (n518). Similarly, CCL18 protein was elevated in NP (4.7561.13 ng/mg, p<0.001, n538) and UT (1.5260.40 ng/mg, p50.066, n529) from CRSwNP compared to UT from CRSsNP (0.5260.06 ng/mg, n532) and control subjects (0.5260.11 ng/mg, n516) in sinonasal tissue. An 8 kDa protein corresponding to CCL18 was detected by western blot only in patients with CRSwNP. Finally, immunofluorescence data showed CCL18 co-localization with CD68 positive macrophages as well as with other un-identified inflammatory cells in NP. CONCLUSIONS: Patients with CRSwNP have elevated levels of CCL18 in NP and UT. The role of CCL18 in the pathogenesis of CRSwNP is worthy of further investigation.