Localized eosinophil degranulation mediates disease in tropical pulmonary eosinophilia.
Laura O'Bryan; Paula Pinkston; Kumaraswami, V.; Vijayan, V.; Gordon Yenokida; Helene F Rosenberg; Ronald Crystal, Eric A Ottesen; Thomas B Nutman.
Infection and Immunity; 2003; 71; 1337-1342.
To explore the mechanism underlying the eosinophil-mediated inflammation of tropical pulmonary eosinophilia (TPE), bronchoalveolar lavage (BAL) fluid, serum and supernatants from pulmonary and blood leukcoytes (WBC) from patients with acute TPE ( n =6) were compared with those obtained from healthy uninfected individuals ( n =4) and from patients with asthma ( n =4) or elephantiasis ( n =5). Although there were no significant differences in the levels of interleukin-4 (IL-4), IL-5, IL-13, eotaxin, granulocyte-macrophage colony-stimulating factor, RANTES, or eosinophil cationic protein, there was a marked increase in eosinophil-derived neurotoxin (EDN) both systemically and in the lungs of individuals with TPE compared to each of the control group (P<0.02). Moreover, there was a compartmentalization of this response, with EDN levels being higher in the BAL fluid than in the serum (P<0.02). Supernatants from WBC from either whole blood or BAL cells were examined for chemokiens, cytokines, eosinophil degranulation products, and arachidonic acid metabolites. Of the many mediators examined - particularly those associated with eosinophil trafficking - only EDN (in BAL fluid and WBC) and MIP-1 a (in WBC) levels were higher for TPE patients than for the non-TPE control groups (P<0.02). These data suggest it is the eosinophilic granular protein EDN, an RNase capable of damaging the lung epithelium, that plays the most important role in the pathogenesis of TPE.
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