This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dondji, B.
Right arrow Articles by Cappello, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dondji, B.
Right arrow Articles by Cappello, M.

 Previous Article  |  Next Article 

Infection and Immunity, June 2008, p. 2560-2567, Vol. 76, No. 6
0019-9567/08/$08.00+0     doi:10.1128/IAI.00094-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Role for Nitric Oxide in Hookworm-Associated Immune Suppression{triangledown}

Blaise Dondji,1 Richard D. Bungiro,1 Lisa M. Harrison,1 Jon J. Vermeire,1 Carlo Bifulco,2 Diane McMahon-Pratt,3,4 and Michael Cappello1,3,4*

Departments of Pediatrics,1 Pathology,2 Microbial Pathogenesis,3 Epidemiology & Public Health, Yale University School of Medicine, New Haven, Connecticut 065204

Received 23 January 2008/ Returned for modification 2 March 2008/ Accepted 9 March 2008

Hookworm infection is a major cause of anemia and malnutrition in resource-poor countries. Human and animal studies suggest that infection with these intestinal nematodes is associated with impaired cellular immunity, characterized by reduced lymphocyte proliferation in response to both parasite and heterologous antigens. We report here data from studies aimed at defining mechanisms through which hookworms modulate the host cellular immune response. Splenocytes and mesenteric lymph node (MLN) cells from hamsters infected with Ancylostoma ceylanicum showed minimal proliferation in response to mitogen at days 20 and 30 postinfection (p.i.), with partial recovery noted at day 70 p.i. The proliferative capacity of enriched splenocyte T-cell preparations from infected animals following stimulation with hookworm antigens was partially restored in the presence of antigen-presenting cells from uninfected hamsters. Analysis by fluorescence-activated cell sorting revealed that hookworm infection is associated with reduced percentages of both CD4+ and surface immunoglobulin G-positive lymphocytes in the spleen and MLN cells. Splenocytes from infected hamsters also secreted more nitric oxide (NO) in culture than did those from naïve animals. Inhibition of NO secretion was associated with partial restoration of the proliferative capacity of splenocytes from infected animals in response to concanavalin A, suggesting a role for NO in mediating this effect. Together, these data demonstrate that hookworm infection is associated with impaired function of antigen-presenting cells and depletion of important lymphocyte subpopulations and also suggests a role for NO in parasite-induced immunosuppression.

* Corresponding author. Mailing address: Yale Child Health Research Center, 464 Congress Avenue, New Haven, CT 06520. Phone: (203) 737-4320. Fax: (203) 737-5972. E-mail: michael.cappello{at}yale.edu

{triangledown} Published ahead of print on 17 March 2008.

Editor: W. A. Petri, Jr.

Infection and Immunity, June 2008, p. 2560-2567, Vol. 76, No. 6
0019-9567/08/$08.00+0     doi:10.1128/IAI.00094-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»