Promoting Open Access to Exploring the Research

Localized Eosinophil Degranulation Mediates Disease in Tropical Pulmonary Eosinophilia

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

[img]
Preview
PDF
200306.pdf - Published Version

Download (120kB)
Official URL: http://iai.asm.org/content/71/3/1337.full.pdf+html

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.

NIRT Creators:
NIRT CreatorsEmail
Item Type: Article
Subjects: Tuberculosis > Clinical Research
Divisions: Clinical Research
Depositing User: Dr. Rathinasabapati R
Date Deposited: 12 Nov 2013 09:43
Last Modified: 09 Mar 2016 10:56
URI: http://eprints.nirt.res.in/id/eprint/600

Actions (login required)

View Item View Item