O'Bryan, L and Pinkston, P and Kumaraswami, V and Vijayan, V and Yenokida, G and Rosenberg, H F and Crystal, R and Ottesen, E A and Nutman, T B
(2003)
Localized Eosinophil Degranulation Mediates Disease in Tropical
Pulmonary Eosinophilia.
Infection and Immunity, 71 (3).
pp. 1337-1342.
ISSN Print: 0019-9567; Online: 1098-5522
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-1� (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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