IL-17-producing peripheral blood CD177+ neutrophils increase in allergic asthmatic subjects

• Published in: Allergy, asthma, and clinical immunology Vol. 9; no. 1; p. 23
• Main Authors: Ramirez-Velazquez, Carlos, Castillo, Elena Cristina, Guido-Bayardo, Leopoldo, Ortiz-Navarrete, Vianney
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 03.07.2013; BioMed Central
• Subjects: Allergy; Asthma; Development and progression; Interleukins; Neutrophils; Physiological aspects; Testing
• ISSN: 1710-1492; 1710-1484; 1710-1492
• DOI: 10.1186/1710-1492-9-23

A T helper cell (TH) 17-biased response has been observed in patients with allergic asthma, particularly in those with neutrophil accumulation in the lung. Therefore, we sought to test the hypothesis that neutrophils might be an important source of interleukin (IL)-17 in allergic asthma. Whole peripheral blood cells from non-asthmatic control subjects (n = 17) and patients with mild asthma (n = 7), moderate but persistent asthma (n = 4), or acute asthma (n = 6) were analyzed for IL-17A expression in CD177+ neutrophils. IL-17A expression was also analyzed in CD3+CD4+ and CD3+CD8+ lymphocyte populations. Asthmatic patients were classified as allergic to fungi, indoor allergens, or other allergens (e.g., pollen) based on a positive intradermal allergy test reaction. The percentage of CD177+ neutrophils in whole blood of asthmatic patients was higher than in healthy controls and highest in the moderate asthma group. Furthermore, the percentage of CD177+IL-17+ neutrophils was elevated in patients with mild asthma, whereas the CD4+ IL-17+ lymphocyte population was higher in asthmatic patients and highest in those with moderate but persistent asthma. We also found that the four patients that were allergic to fungi had the highest percentage of CD177+IL17+ neutrophils and CD8+IL17+ lymphocytes. IL17+CD177+ Neutrophils increase in allergic asthma patients especially when allergic to fungi. This cell population, through release of IL-17, might be contributing during the initial phase asthmatic disease and/or during disease progression but its role has not yet been established.