Nasal biomarkers of immune function differ based on smoking and respiratory disease status

Author:

Rebuli Meghan E.12ORCID,Stanley Lee Anna3,Nurhussien Lina3,Tahir Usman A.3,Sun Wendy Y.3,Kimple Adam J.4,Ebert Charles S.4,Almond Martha2,Jaspers Ilona12ORCID,Rice Mary B.3ORCID

Affiliation:

1. Department of Pediatrics and Curriculum in Toxicology and Environmental Medicine University of North Carolina at Chapel Hill Chapel Hill North Carolina USA

2. Center for Environmental Medicine, Asthma and Lung Biology University of North Carolina at Chapel Hill Chapel Hill North Carolina USA

3. Department of Medicine, Beth Israel Deaconess Medical Center Harvard Medical School Boston Massachusetts USA

4. Department of Otolaryngology‐Head and Neck Surgery University of North Carolina at Chapel Hill Chapel Hill North Carolina USA

Abstract

AbstractRespiratory biomarkers have the potential to identify airway injury by revealing inflammatory processes within the respiratory tract. Currently, there are no respiratory biomarkers suitable for clinical use to identify patients that warrant further diagnostic work‐up, counseling, and treatment for toxic inhalant exposures or chronic airway disease. Using a novel, noninvasive method of sampling the nasal epithelial lining fluid, we aimed to investigate if nasal biomarker patterns could distinguish healthy nonsmoking adults from active smokers and those with chronic upper and lower airway disease in this exploratory study. We compared 28 immune mediators from healthy nonsmoking adults (n = 32), former smokers with COPD (n = 22), chronic rhinosinusitis (CRS) (n = 22), and smoking adults without airway disease (n = 13). Using ANOVA, multinomial logistic regressions, and weighted gene co‐expression network analysis (WGCNA), we determined associations between immune mediators and each cohort. Six mediators (IL‐7, IL‐10, IL‐13, IL‐12p70, IL‐15, and MCP‐1) were lower among disease groups compared to healthy controls. Participants with lower levels of IL‐10, IL‐12p70, IL‐13, and MCP‐1 in the nasal fluid had a higher odds of being in the COPD or CRS group. The cluster analysis identified groups of mediators that correlated with disease status. Specifically, the cluster of IL‐10, IL‐12p70, and IL‐13, was positively correlated with healthy and negatively correlated with COPD groups, and two clusters were correlated with active smoking. In this exploratory study, we preliminarily identified groups of nasal mucosal mediators that differed by airway disease and smoking status. Future prospective, age‐matched studies that control for medication use are needed to validate these patterns and determine if nasosorption has diagnostic utility for upper and lower airway disease or injury.

Funder

Flight Attendant Medical Research Institute

National Heart, Lung, and Blood Institute

National Institute of Environmental Health Sciences

Publisher

Wiley

Subject

Physiology (medical),Physiology

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