An association between neuropeptide Y levels and leukocyte subsets in stress-exacerbated asthmatic mice

Abstract Neuropeptide Y (NPY) was recently proposed to be associated with stress and airway inflammation; however, this has rarely been studied in animal models of asthma. Twenty-four C57BL/6 mice were randomly divided into 3 groups of 8 each: naive control group, asthma group (with an established a...

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Published in:Neuropeptides (Edinburgh) Vol. 57; pp. 53 - 58
Main Authors: Lu, Yanxia, Ho, Roger Chun-Man
Format: Journal Article
Language:English
Published: Netherlands Elsevier Ltd 01-06-2016
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Summary:Abstract Neuropeptide Y (NPY) was recently proposed to be associated with stress and airway inflammation; however, this has rarely been studied in animal models of asthma. Twenty-four C57BL/6 mice were randomly divided into 3 groups of 8 each: naive control group, asthma group (with an established asthma model), and stressed asthma group (with established asthma and stress models). Bronchoalveolar lavage (BAL) fluid was collected for total cell counts using a hemocytometer and for cytological examinations by Wright stain. Differential inflammatory cell counts were performed to identify eosinophils, macrophages, neutrophils, and lymphocytes. NPY and corticosterone serum levels were determined with enzyme immunoassay kits. Stress was associated with increased airway inflammatory response, which was manifested by the accumulation of total leukocytes and eosinophils in the BAL fluid in comparison with the asthma and the control groups. The levels of NPY ( p < 0.05) and corticosterone ( p < 0.01) were elevated in the stressed asthma group in comparison with the control and asthma groups. The concentration of NPY and corticosterone positively correlated with the total leukocyte count ( r = 0.892, p < 0.05 and r = 0.937, p < 0.01 respectively) and eosinophil numbers ( r = 0.806, p = 0.053 and r = 0.885, p < 0.01 respectively). Stress may be associated with elevated peripheral NPY level, which was observed to be associated with exacerbated airway inflammation in asthmatic mice.
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ISSN:0143-4179
1532-2785
DOI:10.1016/j.npep.2015.11.091