Abstract
BackgroundDifferent inflammatory reactions have been observed in the polyp tissues of nonsmokers and smokers with chronic rhinosinusitis (CRS). E-prostanoid (EP) receptors play a role in the inflammatory processes. Cigarette smoke (CS) exposure regulates EP-receptor expression levels promoting inflammatory mediator release from various inflammatory cells. In this study, we characterize the EP-receptor expression profiles in the polyps of nonsmoking and smoking CRS patients to explore the possible role of CS in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP).MethodsPolyp biopsies were obtained from 28 non-smoking and 21 smoking CRSwNP patients. Histopathological characteristics were observed under a light microscope. The prostaglandin E2 (PGE2), TNF-α, and IL-8 contents in polyp tissues were detected using enzyme-linked immunosorbent assay. Immunostaining was used to locate EP receptors in polyps. Messenger RNA and protein expression of EP receptors were examined using quantitative real-time polymerase chain reaction and Western blot, respectively.ResultsMore severe inflammatory reactions occurred in polyp tissues of smoking CRSwNP patients. The PGE2, TNF-α, and IL-8 in tissue homogenate levels were significantly higher in smoking CRSwNP patients than those in nonsmoking CRSwNP patients. Moreover, the distribution of each EP receptor subtype was similar in both groups. Compared with the EP-receptor expression in nonsmokers, messenger RNA and protein of EP2 and EP4 receptor were significantly down-expressed in smoking patients, but EP1 and EP3 receptors did not show significant differences.ConclusionCS exposure downregulates the expression levels of EP2 and EP4 receptors and stimulates the production of PGE2 and the proinflammatory cytokine IL-8 and TNF-α in polyp tissues of CRS patients. The down-expressed EP2 and EP4 receptors might be associated with severe inflammatory reactions in smoking CRSwNP patients.
Highlights
Chronic rhinosinusitis (CRS) is characterized by chronic and persistent inflammation of nasal and paranasal sinus mucosa
More severe inflammatory reactions occurred in polyp tissues of smoking CRS with nasal polyps (CRSwNP) patients
Cigarette smoke (CS) exposure can damage epithelial cells and promote the release of various proinflammatory mediators and inflammatory cell recruitments, thereby leading to numerous inflammatory diseases, such as asthma, emphysema, and chronic obstructive pulmonary diseases [9, 10]. These proinflammatory mediators and infiltrating cells are associated with the development of nasal polyps in CRS patients [4], relatively little is understood whether smoking promotes cell recruitment or causes a change in relevant mediator profiles in nasal polyps to participate in the formation of nasal polyps or CRSwNP
Summary
Chronic rhinosinusitis (CRS) is characterized by chronic and persistent inflammation of nasal and paranasal sinus mucosa. CS exposure can damage epithelial cells and promote the release of various proinflammatory mediators and inflammatory cell recruitments, thereby leading to numerous inflammatory diseases, such as asthma, emphysema, and chronic obstructive pulmonary diseases [9, 10] These proinflammatory mediators and infiltrating cells are associated with the development of nasal polyps in CRS patients [4], relatively little is understood whether smoking promotes cell recruitment or causes a change in relevant mediator profiles in nasal polyps to participate in the formation of nasal polyps or CRSwNP. We characterize the EP-receptor expression profiles in the polyps of nonsmoking and smoking CRS patients to explore the possible role of CS in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP)
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