Abstract

TPS 771: Diet and lifestyle, Exhibition Hall, Ground floor, August 26, 2019, 3:00 PM - 4:30 PM Background: Tobacco exposure has both inflammatory and immunosuppressive effects in the upper and lower respiratory tract. Chronic obstructive pulmonary disease (COPD) is a smoking-related disease characterized by greater susceptibility to infection and abnormal inflammatory responses to noxious particles. We hypothesized that the upper respiratory cytokine milieu of former smokers with COPD would differ from healthy adults with and without tobacco exposure. Methods: We recruited 18 former smokers with moderate to severe COPD, 14 smokers, and 20 non-smokers. We sampled each participant’s nasal epithelial lining fluid using an absorbent fibrous Leukosorb matrix. Soluble immune mediators were eluted and analyzed by multiplex ELISA. We examined 29 inflammatory mediators with relevance to airway disease. Mean concentrations were compared across groups by one-way ANOVA, followed by pair-wise comparisons when differences were found. Results: The concentrations of most biomarkers were similar among former smokers with COPD compared with smokers and non-smokers. However, several biomarkers (IL-7, IL-10, IL-13, IL-12p70, IL-15) differed among the groups (global p<0.05) and all were lower among former smokers with COPD compared to non-smokers. There were no differences between current smokers and former smokers with COPD, but many of these biomarkers were similarly lower among current smokers compared to non-smokers. For example, mean±SD concentration of IL-13 (in pg/mL) was 26.8±17.8 in former smokers with COPD, 32.1±21.3 in smokers, and 70.7±36.9 in non-smokers (global p<0.0001). Conclusions: Certain biomarkers of inflammation and immune status were lower in the nasal epithelial lining fluid of former smokers with COPD compared to non-smokers, but not compared to current smokers. Several biomarkers that differed between the COPD group and non-smokers also differed between current smokers and non-smokers. These findings suggest that alterations in upper respiratory immune defenses in the setting of ongoing smoking may be similar to the sequelae of smoking-related airway disease even after smoking cessation.

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