Group II subfamily secretory phospholipase A2 enzymes:: expression in chronic rhinosinusitis with and without nasal polyps

Background: Group II subfamily secretory phospholipases A(2) (sPLA(2)s) are the enzymes that can play a major role in inflammation. However, the presence of group II subfamily sPLA(2)s in human sinonasal mucosa and their roles in chronic rhinosinusitis (CRS) are not well known. The purpose of this study was to investigate the expression of group II subfamily sPLA(2)s in human sinonasal mucosa from controls and CRS patients with and without nasal polyps (NPs) and the regulation of expression by proinflammatory cytokines. Methods: Surgical samples were investigated by means of reverse transcriptase polymerase chain reaction (RT-PCR) for evaluation of group II subfamily sPLA(2)s mRNA expression, and the presence and location of group II subfamily sPLA(2)s-positive cells were analyzed by means of immunohistochemistry. Furthermore, nasal explant culture and quantitative RT-PCR techniques were used to investigate the effect of interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha on group II subfamily sPLA(2)s mRNA production in sinonasal mucosa. Results: Messenger RNA expression of sPLA(2)-IIA, -IID, and -IIE was significantly upregulated in tissues from CRS patients compared with control tissues. Among CRS patients, patients without NPs showed significantly stronger expression in sinonasal mucosa than patients with NPs of sPLA(2)-IIA mRNA, and weaker expression of sPLA(2)-IIE mRNA. Immunohistochemistry revealed enhanced protein expression of type II sPLA(2)s and specific type IIA sPLA(2) in epithelial cells and submucosal glands in samples from CRS patients. Stronger type IIA sPLA(2) protein expression was found in samples from CRS patients without NPs when compared with NPs. Nasal explant culture experiments demonstrated that mRNA expression of sPLA(2)-IIA, -IID, and -IIE was dramatically induced by IL-1 beta and TNF-alpha. Conclusions: The expression of some members of group II subfamily of sPLA(2)s is upregulated in CRS and it may result from IL-1 beta and TNF-alpha overexpression. Different individual group II subfamily sPLA(2)s may play different roles in the pathogenesis of CRS with and without NPs.