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Articles in PresS, published online ahead of print September 6, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00226.2002
Submitted on July 15, 2002
Accepted on July 24, 2002
1 Unite de Pharmacologie Cellulaire, Institut Pasteur, Paris, France, France
* To whom correspondence should be addressed. E-mail: msinger{at}pasteur.fr.
Intra-tracheal challenges with antigen (OVA)or rmIL-13 induce lung inflammation,bronchial hyperreactivity (BHR)and mucus in mice as independent events (Singer et al, Am. J. Respir. Cell Mol. Biol. 2002, 26, 74-84), largely mediated by leukotrienes (LT). We have previously shown that LTC4 was released 15 min. after Ova, and we show here that it induces the expression of MCP-1, MCP-5, and KC in the lungs, as well as IL-13 mRNAs .Instilled i.t., these chemokines induced BHR and mucus accumulation, which were inhibited by the 5-LO inhibitor zileuton and by the Cys-LT-ra MK-571, suggesting a mediation by cysteinyl-leukotrienes. Since these chemokines also induced LT release into the BALF, and IL-13 in the lungs, we hypothesize that LT- and chemokine-based loops for positive feed-back regulations cooperate to maintain and amplify BHR and lung mucus accumulation, after allergenic challenge, and more largely in situations where IL-13, LT or chemokines are generated.
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