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Stress Enhances Airway Reactivity and Airway Inflammation in an Animal Model of Allergic Bronchial Asthma

Ricarda A. Joachim, MD, David Quarcoo, MD, Petra C. Arck, MD, Udo Herz, PhD, Harald Renz, MD and Burghard F. Klapp, MD

From the Department of Internal Medicine, Charité-Campus Virchow, Humboldt University (R.A.J., P.C.A., B.F.K.), Berlin; Department of Pediatrics, Charité-Campus Virchow, Humboldt University (D.Q.), Berlin; and Department of Clinical Chemistry and Molecular Diagnostic, Philipps-Universität (U.H., H.R.), Marburg, Germany.



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Fig. 1. Experimental protocol. After systemic sensitization on days 0, 14, and 21, OVA IP mice were challenged twice with OVA aerosol on days 26 and 27. Coinciding with the first challenge, the stress group was exposed to sound stress for 24 hours while controls remained undisturbed.

 


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Fig. 2. Effect of stress on AHR measured in OVA-sensitized and airway-challenged CBA/J mice. Indicated are mean and SEM from stressed (N = 8) and nonstressed (N = 8) sensitized CBA/J mice. The frequency that caused 50% of maximal contraction (ES50) was calculated. Airway contractility is expressed as percent of nonstressed control (2.1 Hz). * p < .05.

 


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Fig. 3. Total leukocyte number and cell differentiation in BAL fluid of OVA-sensitized and airway-challenged CBA/J mice. Indicated are mean and SD from stressed (N = 12) and nonstressed (N = 9) sensitized animals (Leukos = leukocytes, Lymphos = lymphocytes, Eos = eosinophil granulocytes, Neutros = neutrophil granulocytes, Mono/Mac=Monocytes/Macrophages). * p < .05.

 





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