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Schistosomal-Derived Lysophosphatidylcholine Are Involved in Eosinophil Activation and Recruitment through Toll-Like Receptor—2—Dependent Mechanisms
Kelly G. Magalhães, Patricia E. Almeida, Georgia C. Atella, Clarissa M. Maya-Monteiro, Hugo C. Castro-Faria-Neto, Marcelo Pelajo-Machado, Henrique L. Lenzi, Marcelo T. Bozza and Patricia T. Bozza
The Journal of Infectious Diseases
Vol. 202, No. 9 (1 November 2010), pp. 1369-1379
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/20790071
Page Count: 11
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Parasite-derived lipids may play important roles in host-pathogen interactions and escape mechanisms. Herein, we evaluated the role of schistosomal-derived lipids in Toll-like receptor (TLR)—2 and eosinophil activation in Schistosoma mansoni infection. Mice lacking TLR2 exhibited reduced liver eosinophilic granuloma, compared with that of wild-type animals, following S. mansoni infection. Decreased eosinophil accumulation and eosinophil lipid body (lipid droplet) formation, at least partially due to reduced production of eotaxin, interleukin (IL)-5, and IL-13 in S. mansoni—infected TLR2 -/- mice, compared with the corresponding production in wild-type mice, was noted. Although no differences were observed in survival rates during the acute schistosomal infection (up to 50 days), increased survival of TLR2 -/- mice, compared with survival of wild-type mice, was observed during the chronic phase of infection. Schistosomal lipid extract— and schistosomal-derived lysophosphatidylcholine (lyso-PC)—stimulated macrophages in vitro induced TLR2-dependent NF-kB activation and cytokine production. Furthermore, in vivo schistosomal lyso-PC administration induced eosinophil recruitment and cytokine production, in a mechanism largely dependent on TLR2. Taken together, our results suggest that schistosomal-derived lyso-PC may participate in cytokine production and eosinophil activation through a TLR2-dependent pathway in S. mansoni infection. Moreover, our results suggest that TLR2-dependent inflammatory reaction, cytokine production, and eosinophil recruitment and activation may contribute to the pathogenesis and lethality in the chronic phase of infection.
The Journal of Infectious Diseases © 2010 Oxford University Press