Akshay Sood1, Clifford Qualls2, JeanClare Seagrave3, Christine Stidley4, Tereassa Archibeque4, Marianne Berwick4, Mark Schuyler4. 1. Department of Medicine, Lovelace Respiratory Research Institute, Albuquerque, NM. Electronic address: asood@salud.unm.edu. 2. Clinical Translational Sciences Center, University of New Mexico School of Medicine, Albuquerque, NM. 3. Experimental Toxicology Program, Lovelace Respiratory Research Institute, Albuquerque, NM. 4. Department of Medicine, Lovelace Respiratory Research Institute, Albuquerque, NM.
Abstract
BACKGROUND: Adiponectin is associated with asthma. The direction of this association is not known in humans. In mice, this association is bidirectional: allergen inhalation affects serum adiponectin, and exogenous adiponectin administration affects asthma. We sought to evaluate whether allergen inhalation affects serum adiponectin in human asthma. METHODS: This study included eight sensitized subjects with mild asthma and six healthy control subjects. Asthmatic subjects were challenged with inhaled specific allergen (positive allergen skin test), methacholine, and irrelevant allergen (negative allergen skin test). Control subjects were challenged with irrelevant allergen. Sequential serum samples were obtained before and nine times after each challenge. Serum adiponectin- (primary outcome), leptin-, adiponectin-to-leptin ratio-, eotaxin-, and tumor necrosis factor-alpha-response curves, area under the curves, and baseline and peak concentrations were evaluated. Statistical analysis used repeated-measures analysis of variance and paired t tests. RESULTS: There were no significant differences in outcome measures among the challenges in asthmatic subjects or when compared to control subjects. Type II error is an unlikely explanation for these findings because the study was adequately powered to detect changes in serum adiponectin, as reported in the literature. Further, pooled data showed that serum adiponectin diurnal variation curves were lower in asthmatic subjects than in control subjects. CONCLUSIONS: Serum adiponectin concentrations are lower in asthmatic subjects than in control subjects. Specific allergen inhalation in asthmatic subjects does not acutely affect serum adiponectin concentrations. The reverse association (ie, effect of adiponectin on asthma) needs further study. If future studies prove adiponectin to be a protective factor for asthma, modulating adiponectin may open a new approach toward managing asthma.
BACKGROUND:Adiponectin is associated with asthma. The direction of this association is not known in humans. In mice, this association is bidirectional: allergen inhalation affects serum adiponectin, and exogenous adiponectin administration affects asthma. We sought to evaluate whether allergen inhalation affects serum adiponectin in humanasthma. METHODS: This study included eight sensitized subjects with mild asthma and six healthy control subjects. Asthmatic subjects were challenged with inhaled specific allergen (positive allergen skin test), methacholine, and irrelevant allergen (negative allergen skin test). Control subjects were challenged with irrelevant allergen. Sequential serum samples were obtained before and nine times after each challenge. Serum adiponectin- (primary outcome), leptin-, adiponectin-to-leptin ratio-, eotaxin-, and tumor necrosis factor-alpha-response curves, area under the curves, and baseline and peak concentrations were evaluated. Statistical analysis used repeated-measures analysis of variance and paired t tests. RESULTS: There were no significant differences in outcome measures among the challenges in asthmatic subjects or when compared to control subjects. Type II error is an unlikely explanation for these findings because the study was adequately powered to detect changes in serum adiponectin, as reported in the literature. Further, pooled data showed that serum adiponectin diurnal variation curves were lower in asthmatic subjects than in control subjects. CONCLUSIONS: Serum adiponectin concentrations are lower in asthmatic subjects than in control subjects. Specific allergen inhalation in asthmatic subjects does not acutely affect serum adiponectin concentrations. The reverse association (ie, effect of adiponectin on asthma) needs further study. If future studies prove adiponectin to be a protective factor for asthma, modulating adiponectin may open a new approach toward managing asthma.
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