Expression Profiles Of ICAM-1 And MCP-1 In Smoking And Non-smoking Nasal Polyps

Background:Recent studies on the etiopathogenesis of nasal polyps have shown that cigarette smoking may cause chronic inflammation of the nasal mucosa and may be associated with nasal polyps. ICAM-1 is a member of the Ig supergene family, which plays an important role in leukocyte trafficking. ICAM-1 upregulation is a signature event during inflammation. Chemokines play a major role in selectively recruiting neutrophils, monocytes, and lymphocytes. MCP-1 is one of the key chemokines that regulate migration and infiltration of monocytes/macrophages. However, until now there was still no report about the expression profiles of ICAM-1 and MCP-1 in smoking and non-smoking nasal polyps Objective:The purpose of the study was to explore the effects of smoking on nasal polyp histopathology, to investigate the expression profiles of ICAM-1 and MCP-1 in smoking and non-smoking nasal polyps and to illustrate the relationship between smoking and the formation of nasal polyps. Methods:Nasal biopsies were obtained from 21 smoking nasal polyps,22 non-smoking nasal polyps patients, 10 smoking control and 10 non-smoking control. Histopathologic characteristics were observed under a light microscope. The light microscopic findings of the following seven histopathologic characteristics were compared in the smoking and non-smoking nasal polyps groups: the thickness of the basement membrane, subepithelial edema, submucous gland formation, goblet cell hyperplasia, lymphocyte, PMNs infiltration and inflammatory cells. ICAM-1 and MCP-1 expression levels were determined by immunohistochemical analysis. Results:Under the light microscopy, we found that both smoking and non-smoking nasal polyps showed gland formation, goblet cell hyperplasia, the thickness of the basement membrane, subepithelial edema, and inflammatory cell infiltration. No statistically significant differences were found between smoker and non-smoker groups with regard to the histopathological findings, which suggested that in our study cigarette smoking did not make a significant difference in histopathological characteristics of nasal polyps.Both smoking and non-smoking nasal polyps showed positive expression of ICAM-1 and MCP-1 by immunohistochemical staining. ICAM-1 expression was predominantly observed in the basal epithelial layer,activated vascular endothelium and inflammatory cells. And MCP-1 was mainly expressed in the epithelium, nasal glands and inflammatory cells. Whereas ICAM-1 and MCP-1 expression are constitutively low in healthy group.Whether smoking or not, both ICAM-1 and MCP-1 showed significant immunostaining of nasal polyps compared with the healthy controls(P<0.001). However, there are no statistically significant differences between smoker and non-smoker nasal polyps groups((P>0.05). Conclusion:We did not find any statistically significant differences in histopathological characteristics of nasal polyps between smoker and non-smoker groups. ICAM-1 and MCP-1 were associated with nasal polyps remodeling, and the body itself may actively participate in the inflammation of nasal polyps by upregulating the expression of ICAM-1 and MCP-1.