Localized eosinophil degranulation mediates disease in tropical pulmonary eosinophilia.

Abstract:

:To explore the mechanisms underlying the eosinophil-mediated inflammation of tropical pulmonary eosinophilia (TPE), bronchoalveolar lavage (BAL) fluid, serum, and supernatants from pulmonary and blood leukocytes (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 groups (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 chemokines, 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-1alpha (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.

journal_name

Infect Immun

journal_title

Infection and immunity

authors

O'Bryan L,Pinkston P,Kumaraswami V,Vijayan V,Yenokida G,Rosenberg HF,Crystal R,Ottesen EA,Nutman TB

doi

10.1128/iai.71.3.1337-1342.2003

keywords:

subject

Has Abstract

pub_date

2003-03-01 00:00:00

pages

1337-42

issue

3

eissn

0019-9567

issn

1098-5522

journal_volume

71

pub_type

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