| Objective: The study was aimed to investigate the role of the lipoxin A4?LXA4?and lipoxin A4 receptor?ALXR? in the epithelial-mesenchymal transition of Chronic rhinosinusitis, which wound further explore the pathogenesis of tissue remodeling in Chronic rhinosinusitis.Method:?1? The change of Lipoxin A4 receptor expressed in nasal mucosa was detected in patients with chronic rhinosinusitis by immunohistochemistry, RT-PCR and Western blot.?2? Nasal mucosa epithelial cells?HNEp C? were cultured in vitro,and transformed into mesenchymal cells induced by the different concentrations of TGF-?1?0? 0.1? 1?10? 100 ng/m L?. LXA4 of different concentrations?0?1?10 ? 100 ? 200 n M? were added in respectively after the impact of TGF-?1 for30 minutes. The cell morphological changes were observed under phase contrast microscope. ?-SMA and E-cadherin on cell surface were measured by RT-PCR and Western blot, and collagen ? was detected by ELISA kit in cell cu Lture supernatant liquor. BOC-2, antagonistic on the ALXR, was added in HNEp C in advance for 30 minutes, and then LXA4 and the TGF-?1 were added in in turn, then the changes in HNEp C was observed.Results:?1? Immunohistochemical results showed ALXR was expressed in the epithelium of mucosa and glands, and strongly expressed in patients with chronic rhinosinusitis.. The result of RT-PCR and Western blot showed that ALXR in patients with chronic rhinosinusitis was higher than that of patients without chronic sinusitis, while the expression in patients with CRSw NP was lower than that with CRSs NP, and these differences were significant?P < 0.05?.?2? TGF-?1 of different concentrations could induce HNEp C to convert into muscle fibroblasts, and as a result, the function, morphology and surface marker of nasal mucosal epithelial cells changed. The connection between epithelium was interrupted induced by TGF-?1 at 120 h, and some cells changed from flat to long spindle. E-cadherin, the epithelial marker, was lowely expressed and ?-SMA symboling mesenchymal cells was high expressed. The amount of collagen ? deposited in culture dish was also increased gradually with the extension of observation time.?3? LXA4 in different concentrations could inhibited that TGF-?1 induced epithelium to convert into mesenchymal cells in nasal mucosa, and prevented cells into fusiformis and the expression of ?-SMA in cell surface. BOC-2 antagonistic on the ALXR could reduce the inhibitory effect of LXA4, which showed the inhibitory effect of LXA4 on EMT induced by TGF-?1 came true at least partly by up-regulation of the receptor.Conclusion:?1? The ALXR was highly expressed in patients with chronic rhinosinusitis.?2? The TGF-?1 at certain concentrations could induce nasal mucosa epithelial cells to convert into muscle fibroblasts, and the function, morphology and surface marker of cell changed.?3? LXA4 at certain concentrations could inhibit EMT in nasal mucosa by TGF-?1 via its receptor ALXR.?4? LXA4 and ALXR might be closely related to the pathological and physiological process in occurrence and development of chronic rhinosinusitis. |
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