title: Association between airway hyperreactivity and bronchial macrophage dysfunction in individuals with mild asthma.
abstract: Little is known about the functional capabilities of bronchial macrophages (BMs) and their relationship to airway disease such as asthma. We hypothesize that BMs from asthmatics may be modulated in their function compared with similar cells from healthy individuals. BMs obtained by induced sputum from mild asthmatics (n = 20) and healthy individuals (n = 20) were analyzed using flow cytometry for CD16, CD64, CD11b, CD14, and human leukocyte antigen-DR expression, phagocytosis of IgG opsonized yeast, and oxidant production. Asthma status was assessed by lung function [percent predicted forced vital capacity and forced expiratory volume in 1 s (FEV(1))], percent sputum eosinophils, and nonspecific airway responsiveness [provocative concentration that produces a 20% fall in FEV(1) (PC(20,FEV1))]. Asthmatics with >5% airway eosinophils (AEo+) had decreased BM CD64 expression and phagocytosis compared with asthmatics with <5% eosinophils (AEo-). Among asthmatics, a significant correlation was found between CD64 expression and BM phagocytosis (R = 0.7, P < 0.009). Phagocytosis was also correlated with PC(20,FEV1) (R = 0.6, P < 0.007), lung function (%predicted FEV(1), R = 0.7, P < 0.002) and percent eosinophils (R = -0.6, P < 0.01). In conclusion, BM from asthmatics are functionally modulated, possibly by Th2 cytokines involved in asthma pathology.
authors.affiliation: Center For Environmental Medicine and Lung Biology, University of North Carolina, Chapel Hill 27599, North Carolina, USA. Neil_Alexis@med.unc.edu
authors.forename: N E
authors.initials: NE
authors.lastname: Alexis
authors.forename: J
authors.initials: J
authors.lastname: Soukup
authors.forename: S
authors.initials: S
authors.lastname: Nierkens
authors.forename: S
authors.initials: S
authors.lastname: Becker
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000032:analysis / Q000378:metabolism; D001249:Asthma / Q000276:immunology / Q000473:pathology; D001798:Blood Proteins / Q000378:metabolism; D001980:Bronchi / Q000276:immunology* / Q000473:pathology; D016207:Cytokines / Q000378:metabolism; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D006684:HLA-DR Antigens / Q000032:analysis / Q000378:metabolism; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007958:Leukocyte Count; D016014:Linear Models; D016676:Macrophages, Alveolar / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D008297:Male; D016877:Oxidants / Q000378:metabolism; D010587:Phagocytosis / Q000276:immunology; D012129:Respiratory Function Tests; D012130:Respiratory Hypersensitivity / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D012260:Ribonucleases; D012720:Severity of Illness Index; D013183:Sputum / Q000166:cytology / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism; D015003:Yeasts / Q000276:immunology
chemical_list: D015703:Antigens, CD; D001798:Blood Proteins; D016207:Cytokines; D047091:Eosinophil Granule Proteins; D006684:HLA-DR Antigens; D007074:Immunoglobulin G; D016877:Oxidants; D012260:Ribonucleases