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Am. J. Trop. Med. Hyg., 75(6), 2006, pp. 1053-1057
Copyright © 2006 by The American Society of Tropical Medicine and Hygiene

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SHORT REPORT


HIGHER PERCENTAGES OF CIRCULATING MAST CELL PRECURSORS CORRELATE WITH SUSCEPTIBILITY TO REINFECTION WITH SCHISTOSOMA MANSONI

LISA M. GANLEY-LEAL, PAULINE N. M. MWINZI, CATHERINE B. CETRE-SOSSAH, JULIUS ANDOVE, ALLEN W. HIGHTOWER, DIANA M. S. KARANJA, DANIEL G. COLLEY, AND W. EVAN SECOR*
Centers for Disease Control and Prevention, Division of Parasitic Diseases, Atlanta, Georgia; Kenya Medical Research Institute, Centre for Vector Biology and Control Research, Kisumu, Kenya; Center for Tropical & Emerging Global Diseases, and the Department of Microbiology, University of Georgia, Athens, GA; Division of Infectious Diseases, Boston University School of Medicine, Boston, MA

 

ABSTRACT

A high level of serum IgE is generally associated with human resistance to schistosomes, though the protective mechanisms of IgE remain undefined. We recently reported that whereas some individuals who are occupationally hyperexposed to Schistosoma mansoni display resistance to reinfection, others remain highly susceptible, in some cases due to HIV-1 co-infection. As IgE functions, in part, through Fc{varepsilon}RI on mast cells, we characterized circulating CD117+ Fc{varepsilon}RI+ mast cell precursors in this population. Surprisingly, a higher percentage of CD117+ cells correlated with a susceptible phenotype in HIV-1 seronegative participants with schistosomiasis. There was no association between percentages of peripheral CD117+ cells and susceptibility to reinfection in persons with HIV-1. Serum levels of polyclonal IgE were inversely correlated with percentages of CD117+ cells regardless of HIV-1 status. Thus, immature mast cells may affect IgE availability, or IgE may affect immature mast cells, altering the balance of host susceptibility and resistance to schistosomes.

Received June 19, 2006. Accepted for publication August 14, 2006.

Acknowledgments The authors thank Karen Wozniak for critical review of this manuscript, Kennedy Matuda for stool evaluation, and especially all the study participants. This study is published with the permission of the Director, Kenya Medical Research Institute. The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention.

Financial support: LMG was supported by the American Society of Microbiology/National Center for Infectious Disease Postdoctoral Fellowship (2000–2002) and by T32 AI52070 (2003–2006) and CCS by Fondation pour la Recherche Médicale. This work was supported in part by NIH AI053695.

* Address correspondence to W. Evan Secor, Division of Parasitic Diseases, Centers for Disease Control and Prevention, 4770 Buford Highway, Mailstop F-13, Atlanta, GA 30341. E-mail: was4{at}cdc.gov

Authors’ addresses: Lisa M. Ganley-Leal, Division of Infectious Diseases, Boston University School of Medicine, Boston, MA, E-mail: Lisa.GanleyLeal{at}bmc.org. Pauline N.M. Mwinzi, Diana M.S. Karanja, and Julius Andove, Vector Biology and Control Research Centre, Kenya Medical Research Institute, PO Box 1578, Kisumu, Kenya, E-mails: pmwinzi{at}kisian.mimcom.net and dkaranja{at}kisian.mimcom.net. Catherine B. Cetre-Sossah, CIRAD, Campus International de Baillarguet, Montpellier, France, E-mail: catherine.cetre-sossah{at}cirad.fr. Daniel G. Colley, Center for Tropical and Emerging Global Diseases, Room 145, Coverdell Center, University of Georgia, Athens, GA 30602, E-mail: dcolley{at}uga.edu. Allen W. Hightower and W. Evan Secor, Division of Parasitic Diseases, Centers for Disease Control and Prevention, 4770 Buford Highway, Mail-stop F-13, Atlanta, GA 30341, E-mails: ahightower{at}ke.cdc.gov and was4{at}cdc.gov.




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Copyright © 2006 by the American Society of Tropical Medicine and Hygiene.