2010 OPEN FORUM Abstracts
INCREASES IN AIRWAY EOSINOPHILIA AND A TH1 CYTOKINE DURING THE CHRONIC ASYMPTOMATIC PHASE IN PATIENTS WITH ASTHMA.
Chang-Keun Kim1, Gerald Volcheck2, Hirohito Kita2; 1Asthma Allergy Center, Inje University-Sanggyepaik Hospital, Seoul, Republic of Korea; 2Department of Immunology, Mayo Clinic and Foundation,, Rochester, MN
Background: Previous studies, using allergen asthma challenge models or measurements during acute asthma exacerbations, have suggested roles for the Th2 cytokines in promoting airway inflammation in asthma patients. We assessed mediators of airway inflammation during the chronic asymptomatic phase of asthma. Methods: Nine nonatopic asthma (NAA) patients, 19 atopic asthma (AA) patients, 20 atopic controls (AC), and 38 normal controls (NC) underwent sputum induction when asymptomatic. Sputum total cell counts and differentials were determined; levels of the cytokines, IL-4, IL-5, IL-13, GM-CSF, IFN-g, and the chemokines, eotaxin and RANTES, were measured by ELISA; and the levels of eosinophil-derived neurotoxin (EDN) were measured by radioimmunoassay(RIA). Results: NAA and AA patients showed a higher percentage of sputum eosinophils compared to AC (P < 0.001) and NC (P < 0.0001); furthermore, NAA patients showed higher percentage of sputum eosinophils and total eosinophils compared to AA (P < 0.01). Similarly, NAA and AA patients showed higher sputum EDN levels compared to AC (P < 0.01 and P < 0.05) and NC (P < 0.01). No differences were observed in the sputum levels of IL-4, IL-5, and IL-13 among the four groups. In contrast, the IFN-g levels were higher in NAA (P < 0.001) and AA(P < 0.0001) patients compared to AC and NC. Interestingly, the GM-CSF levels were higher in AA (P < 0.01) patients compared to AC or NC. NAA (P < 0.01) patients showed higher eotaxin levels compared to AA, AC, and NC; NAA and AA patients showed higher RANTES levels compared to NC (P < 0.05). In NAA, AA, and AC patients, the percentage of sputum eosinophils and EDN levels correlated positively with the levels of IFN-g(r=0.606 and p < 0.0001, r=0.432 and p < 0.01), GM-CSF(r=0.541 and p < 0.0001, r=0.453 and p < 0.01), eotaxin (r=0.640 and p < 0.0001, r=0.514 and p < 0.001), and RANTES (r=0.506 and p < 0.001, r=0.480 and p < 0.001), but not with the IL-5 levels. Conclusions: The baseline airway inflammation of asthma, irrespective of an atopic or nonatopic diathesis, is characterized by eosinophilic inflammation and a Th1 cytokine, IFN-g. GM-CSF, instead of IL-5, and chemokines may coordinate airway eosinophilia during the chronic phase of asthma. Sponsored Research - None