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Infection and Immunity, November 2001, p. 6755-6768, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.6755-6768.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Patterns of Chemokine Expression in Models of Schistosoma mansoni Inflammation and Infection Reveal Relationships between Type 1 and Type 2 Responses and Chemokines In Vivo

Matthew K. Park,1 Karl F. Hoffmann,2 Allen W. Cheever,3 Doron Amichay,1 Thomas A. Wynn,2,* and Joshua M. Farber1,*

Laboratory of Clinical Investigation1 and Schistosomiasis Immunology and Pathology Unit, Immunobiology Section, Laboratory of Parasitic Diseases,2 National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, and The Biomedical Research Institute, Rockville, Maryland 208523

Received 28 March 2001/Returned for modification 2 May 2001/Accepted 3 August 2001

To explore the roles of chemokines in type 1 and type 2 responses in vivo, we examined mRNA expression for a panel of up to 17 chemokines in experimental mouse models using Schistosoma mansoni. These studies revealed that Mig (monokine induced by gamma interferon), cytokine-responsive gene 2/10-kDa interferon-inducible protein, RANTES, lymphotactin, macrophage inflammatory protein 1beta (MIP-1beta ), JE/monocyte chemoattractant protein 1, and MIP-2 are associated with type 1 egg-induced responses and that thymus-derived chemotactic agent 3 (TCA3), eotaxin, MIP-1alpha , and MIP-1gamma are associated with type 2 egg-induced responses. After cercarial infection, both type 1-associated and type 2-associated chemokines were elevated in the livers of infected mice presensitized with eggs and recombinant interleukin-12 (rIL-12), a regimen that diminishes pathology. Neutralization of IL-12 or gamma interferon during egg deposition reversed the effects of prior treatment with rIL-12, leading to a return to larger granulomas; persistently elevated expression of TCA3, eotaxin, and MIP-1alpha ; and a marked reduction in the expression of type 1-associated chemokines despite the maintenance of a dominant type 1 cytokine response in the draining lymph nodes. Our findings suggest that there are patterns of coordinate chemokine expression characteristic of type 1 and type 2 responses in vivo; that the cells recruited by a given pattern of chemokines may differ, depending on the composition of peripheral populations; and that patterns of tissue expression of chemokines may determine the character of an inflammatory response independently of the dominant pattern of differentiation of antigen-specific T cells. Our data reveal new relationships between chemokines and polarized immune responses and suggest that end organ inflammation might be altered by chemokine blockade without necessitating reversal of the phenotype of the majority of differentiated T cells.

* Corresponding author. Mailing address for Joshua M. Farber: Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bldg. 10, Rm. 11N228, MSC-1888, Bethesda, MD 20892-1888. Phone: (301) 402-4910. Fax: (301) 402-0627. E-mail: jfarber{at}niaid.nih.gov. Mailing address for Thomas A. Wynn: Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bldg. 4, Rm. 126, MSC-0425, Bethesda, MD 20892-0425. Phone: (301) 496-4758. Fax: (301) 402-0077. E-mail: twynn{at}atlas.niaid.nih.gov.

Infection and Immunity, November 2001, p. 6755-6768, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.6755-6768.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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