Background: Group II subfamily secretory phospholipases A2 (sPLA2s) are the enzymes that can play a major role in inflammation. However, the presence of group II subfamily sPLA2s 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 sPLA2s 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 sPLA2s mRNA expression, and the presence and location of group II subfamily sPLA2s-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)-1β and tumor necrosis factor (TNF)-α on group II subfamily sPLA2s mRNA production in sinonasal mucosa.
Results: Messenger RNA expression of sPLA2-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 sPLA2-IIA mRNA, and weaker expression of sPLA2-IIE mRNA. Immunohistochemistry revealed enhanced protein expression of type II sPLA2s and specific type IIA sPLA2 in epithelial cells and submucosal glands in samples from CRS patients. Stronger type IIA sPLA2 protein expression was found in samples from CRS patients without NPs when compared with NPs. Nasal explant culture experiments demonstrated that mRNA expression of sPLA2-IIA, -IID, and -IIE was dramatically induced by IL-1β and TNF-α.
Conclusions: The expression of some members of group II subfamily of sPLA2s is upregulated in CRS and it may result from IL-1β and TNF-α overexpression. Different individual group II subfamily sPLA2s may play different roles in the pathogenesis of CRS with and without NPs.