Journal of Experimental Medicine, Vol 183, 109-117, Copyright © 1996 by Rockefeller University Press

ARTICLES

Interleukin 4, but not interleukin 5 or eosinophils, is required in a murine model of acute airway hyperreactivity [published erratum appears in J Exp Med 1997 May 5;185(9):1715]

DB Corry, HG Folkesson, ML Warnock, DJ Erle, MA Matthay, JP Wiener-Kronish and RM Locksley
Department of Medicine, University of California San Francisco 94143- 0654, USA.

Reversible airway hyperreactivity underlies the pathophysiology of asthma, yet the precise mediators of the response remain unclear. Human studies have correlated aberrant activation of T helper (Th) 2-like effector systems in the airways with disease. A murine model of airway hyperreactivity in response to acetylcholine was established using mice immunized with ovalbumin and challenged with aerosolized antigen. No airway hyperractivity occurred in severe combined immunodeficient mice. Identically immunized BALB/c mice developed an influx of cells, with a predominance of eosinophils and CD4+ T cells, into the lungs and bronchoalveolar lavage fluid at the time that substantial changes in airway pressure and resistance were quantitated. Challenged animals developed marked increases in Th2 cytokine production, eosinophil influx, and serum immunoglobulin E levels. Neutralization of interleukin (IL) 4 using monoclonal antibodies administered during the period of systemic immunization abrogated airway hyperractivity but had little effect on the influx of eosinophils. Administration of anti-IL-4 only during the period of the aerosol challenge did not affect the subsequent response to acetylcholine. Finally, administration of anti- IL-5 antibodies at levels that suppressed eosinophils to < 1% of recruited cells had no effect on the subsequent airway responses. BALB/c mice had significantly greater airway responses than C57BL/6 mice, consistent with enhanced IL-4 responses to antigen in BALB/c mice. Taken together, these data implicate IL-4 generated during the period of lymphocyte priming with antigen in establishing the cascade of responses required to generate airway hyperractivity to inhaled antigen. No role for IL-5 or eosinophils could be demonstrated.
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• SALVI, S. S., SURESH BABU, K., HOLGATE, S. T. (2001). Is Asthma Really Due to a Polarized T Cell Response Toward a Helper T Cell Type 2 Phenotype?. Am. J. Respir. Crit. Care Med. 164: 1343-1346 [Full Text]  
• Drouin, S. M., Corry, D. B., Kildsgaard, J., Wetsel, R. A. (2001). Cutting Edge: The Absence of C3 Demonstrates a Role for Complement in Th2 Effector Functions in a Murine Model of Pulmonary Allergy. J. Immunol. 167: 4141-4145 [Abstract] [Full Text]  
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• Hertz, M., Mahalingam, S., Dalum, I., Klysner, S., Mattes, J., Neisig, A., Mouritsen, S., Foster, P. S., Gautam, A. (2001). Active Vaccination Against IL-5 Bypasses Immunological Tolerance and Ameliorates Experimental Asthma. J. Immunol. 167: 3792-3799 [Abstract] [Full Text]  
• Borchers, M. T., Crosby, J., Justice, P., Farmer, S., Hines, E., Lee, J. J., Lee, N. A. (2001). Intrinsic AHR in IL-5 transgenic mice is dependent on CD4+ cells and CD49d-mediated signaling. Am. J. Physiol. Lung Cell. Mol. Physiol. 281: L653-L659 [Abstract] [Full Text]  
• Takaoka, A., Tanaka, Y., Tsuji, T., Jinushi, T., Hoshino, A., Asakura, Y., Mita, Y., Watanabe, K., Nakaike, S., Togashi, Y., Koda, T., Matsushima, K., Nishimura, T. (2001). A Critical Role for Mouse CXC Chemokine(s) in Pulmonary Neutrophilia During Th Type 1-Dependent Airway Inflammation. J. Immunol. 167: 2349-2353 [Abstract] [Full Text]  
• Kanwar, S., Smith, C. W., Shardonofsky, F. R., Burns, A. R. (2001). The Role of Mac-1 (CD11b/CD18) in Antigen-Induced Airway Eosinophilia in Mice. Am. J. Respir. Cell Mol. Bio. 25: 170-177 [Abstract] [Full Text]  
• Renauld, J-C (2001). New insights into the role of cytokines in asthma. J. Clin. Pathol. 54: 577-589 [Abstract] [Full Text]  
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• Kips, J.C. (2001). Cytokines in asthma. Eur Respir J 18: 24S-33s [Abstract] [Full Text]  
• Chapman, J. T., Otterbein, L. E., Elias, J. A., Choi, A. M. K. (2001). Carbon monoxide attenuates aeroallergen-induced inflammation in mice. Am. J. Physiol. Lung Cell. Mol. Physiol. 281: L209-L216 [Abstract] [Full Text]  
• Finotto, S., De Sanctis, G. T., Lehr, H. A., Herz, U., Buerke, M., Schipp, M., Bartsch, B., Atreya, R., Schmitt, E., Galle, P. R., Renz, H., Neurath, M. F. (2001). Treatment of Allergic Airway Inflammation and Hyperresponsiveness by Antisense-Induced Local Blockade of Gata-3 Expression. JEM 193: 1247-1260 [Abstract] [Full Text]  
• Tournoy, K. G., Kips, J. C., Pauwels, R. A. (2001). The Allergen-Induced Airway Hyperresponsiveness in a Human-Mouse Chimera Model of Asthma Is T Cell and IL-4 and IL-5 Dependent. J. Immunol. 166: 6982-6991 [Abstract] [Full Text]  
• Russo, M., Nahori, M.-A., Lefort, J., Gomes, E., de Castro Keller, A., Rodriguez, D., Ribeiro, O. G., Adriouch, S., Gallois, V., de Faria, A. M. C., Vargaftig, B. B. (2001). Suppression of Asthma-like Responses in Different Mouse Strains by Oral Tolerance. Am. J. Respir. Cell Mol. Bio. 24: 518-526 [Abstract] [Full Text]  

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