title: Siglec-8 in induced sputum of COPD patients.
abstract: Chronic obstructive pulmonary disease (COPD) is related to infiltration and activation of inflammatory cells in airways and pulmonary tissue. In COPD, neutrophils are prominent, while eosinophilic influx is typical to asthma. Inflammatory cells express sialic acid-binding immunoglobulin like lectins called Siglecs, a family of innate immune receptors that are transmembrane I-type lectins binding sialic acid. One member of the Siglec family, Siglec-8, is expressed mostly in eosinophils and may be an important therapeutic target in asthma or COPD. The aim of our project was to quantify Siglec-8 expression in induced sputum cells of COPD patients treated with long-acting beta2-agonists (LABA) or combined with long-acting antimuscarinic agents (LAMA) - tiotropium bromide. Thirty stable COPD patients (21 males and 9 females, mean age 67 years) receiving 12 μg BID formoterol therapy were assessed before and after 3 months' add-on therapy consisting of 18 μg QID tiotropium. In all patients, spirometry, lung volumes, and DLCO were performed before and after therapy. The patients were subjected to sputum induction before and after therapy. Sputum cells were isolated and processed to obtain cell membranes. Siglec-8 protein expression was assessed using Western blot. In patients receiving tiotropium and formoterol, improved FEV1 and lung volumes were observed compared with formoterol-only treated patients. The mean Siglec-8 level was significantly higher in eosinophilic subgroup of COPD patients compared with non-eosinophilic patients before therapy 40,000 vs. 15,000 Adj. Vol. INT/mm(2). Our data show that Siglec-8 may be involved in COPD pathogenesis and may influence COPD phenotyping.
authors.affiliation: Department of Chest Diseases and Tuberculosis, Bialystok Medical University, 14 Zurawia St., Bialystok, Poland, robmroz@wp.pl.
authors.forename: R M
authors.initials: RM
authors.lastname: Mroz
authors.forename: A
authors.initials: A
authors.lastname: Holownia
authors.forename: P
authors.initials: P
authors.lastname: Wielgat
authors.forename: A
authors.initials: A
authors.lastname: Sitko
authors.forename: T
authors.initials: T
authors.lastname: Skopinski
authors.forename: E
authors.initials: E
authors.lastname: Chyczewska
authors.forename: J J
authors.initials: JJ
authors.lastname: Braszko
mesh_terms: D058666:Adrenergic beta-2 Receptor Agonists / Q000378:metabolism*; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism*; D000944:Antigens, Differentiation, B-Lymphocyte / Q000378:metabolism*; D004338:Drug Combinations; D004804:Eosinophils / Q000378:metabolism; D004983:Ethanolamines / Q000008:administration & dosage; D005260:Female; D000068759:Formoterol Fumarate; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation; D037102:Lectins / Q000378:metabolism*; D008297:Male; D010641:Phenotype; D029424:Pulmonary Disease, Chronic Obstructive / Q000188:drug therapy / Q000378:metabolism*; D012602:Scopolamine Derivatives / Q000008:administration & dosage; D013183:Sputum / Q000378:metabolism*; D000069447:Tiotropium Bromide
chemical_list: D058666:Adrenergic beta-2 Receptor Agonists; D015703:Antigens, CD; D000944:Antigens, Differentiation, B-Lymphocyte; D004338:Drug Combinations; D004983:Ethanolamines; D037102:Lectins; C403967:SIGLEC8 protein, human; D012602:Scopolamine Derivatives; D000068759:Formoterol Fumarate; D000069447:Tiotropium Bromide