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Title

The coordinated action of CC chemokines in the lung orchestrates allergic inflammation and airway hyperresponsiveness

AuthorsGonzalo, José Ángel; Lloyd, Clare M.; Wen, Danyi; Albar, Juan Pablo; Wells, Timothy N.C.; Proudfoot, Amanda; Martínez-Alonso, Carlos; Gutiérrez Ramos, José Carlos
KeywordsChemokines
Allergic inflammation
Bronchial hyperresponsiveness
Issue DateJul-1998
PublisherRockefeller University Press
CitationThe Journal of Experimental Medicine, volume 188, number 1, July 6, 1998, pp. 157–167
AbstractThe complex pathophysiology of lung allergic inflammation and bronchial hyperresponsiveness (BHR) that characterize asthma is achieved by the regulated accumulation and activation of different leukocyte subsets in the lung. The development and maintenance of these processes correlate with the coordinated production of chemokines. Here, we have assessed the role that different chemokines play in lung allergic inflammation and BHR by blocking their activities in vivo. Our results show that blockage of each one of these chemokines reduces both lung leukocyte infiltration and BHR in a substantially different way. Thus, eotaxin neutralization reduces specifically BHR and lung eosinophilia transiently after each antigen exposure. Monocyte chemoattractant protein (MCP)-5 neutralization abolishes BHR not by affecting the accumulation of inflammatory leukocytes in the airways, but rather by altering the trafficking of the eosinophils and other leukocytes through the lung interstitium. Neutralization of RANTES (regulated upon activation, normal T cell expressed and secreted) receptor(s) with a receptor antagonist decreases significantly lymphocyte and eosinophil infiltration as well as mRNA expression of eotaxin and RANTES. In contrast, neutralization of one of the ligands for RANTES receptors, macrophage-inflammatory protein 1 a , reduces only slightly lung eosinophilia and BHR. Finally, MCP-1 neutralization diminishes drastically BHR and inflammation, and this correlates with a pronounced decrease in monocyte- and lymphocyte-derived inflammatory mediators. These results suggest that different chemokines activate different cellular and molecular pathways that in a coordinated fashion contribute to the complex pathophysiology of asthma, and that their individual blockage results in intervention at different levels of these processes.
DescriptionCopyright by The Rockefeller University Press
URIhttp://hdl.handle.net/10261/3634
ISSN0022-1007
Appears in Collections:(CNB) Artículos
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