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Infection and Immunity, November 2002, p. 5903-5912, Vol. 70, No. 11
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.11.5903-5912.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Enhanced Interleukin-12 and CD40 Ligand Activities but Reduced Staphylococcus aureus Cowan 1-Induced Responses Suggest a Generalized and Progressively Impaired Type 1 Cytokine Pattern for Human Schistosomiasis

Silvia M. L. Montenegro,1 Frederico G. C. Abath,1 Ana Lúcia C. Domingues,2 Wlademir G. Melo,1 Clarice N. L. Morais,1 Eridan M. Coutinho,1 Siddhartha Mahanty,3 and Thomas A. Wynn4*

Departamento de Imunologia, Centro de Pesquisas Aggeu Magalhães-FIOCRUZ,1 Universidade Federal de Pernambuco, Recife, Brazil,2 Centers for Disease Control and Prevention, Atlanta, Georgia,3 Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland4

Received 2 January 2002/ Returned for modification 24 April 2002/ Accepted 6 August 2002

Whole-blood-cell cultures from schistosomiasis patients were stimulated with a variety of T-cell-dependent and T-cell-independent stimuli to determine whether the defect in type 1 cytokine expression observed following helminth infection is associated with alterations in interleukin-12 (IL-12) or CD40 ligand (CD40L) responsiveness. Cultures from uninfected individuals produced abundant gamma interferon in response to Staphylococcus aureus Cowan 1 (SAC), while patients with intestinal and hepatosplenic disease displayed intermediate and weak responses, respectively. Importantly, the decrease in type 1 cytokine expression was not attributed to defects in IL-12- or CD40L-induced activity. Indeed, schistosomiasis patients displayed heightened responses and even produced more biologically active IL-12 when stimulated with SAC and CD40L than did uninfected controls. Finally, additional studies suggested only a partial role for IL-10, since intestinal patients were the only group that overproduced this downregulatory cytokine. Together, these studies demonstrate that the type 1 deficiency in chronic hepatosplenic schistosomiasis is not related to specific defects in IL-12, IL-10, or CD40L activity, although changes in the functional status of antigen-presenting cells appear to be involved.

* Corresponding author. Mailing address: Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, MSC 8003, Room 6154, 50 South Dr., Bethesda, MD 20892. Phone: (301) 496-4758. Fax: (301) 402-0890. E-mail: twynn{at}niaid.nih.gov.

Editor: J. M. Mansfield

Infection and Immunity, November 2002, p. 5903-5912, Vol. 70, No. 11
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.11.5903-5912.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.





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