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Infection and Immunity, April 2002, p. 2090-2099, Vol. 70, No. 4
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.4.2090-2099.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Role of Gamma Interferon in Chemokine Expression in the Ileum of Mice and in a Murine Intestinal Epithelial Cell Line after Cryptosporidium parvum Infection

Laboratoire de Protozoologie, Unité de Pathologie Aviaire et de Parasitologie, INRA de Tours, 37380 Nouzilly, France

Received 26 July 2001/ Returned for modification 27 August 2001/ Accepted 3 December 2001

Cryptosporidium parvum is a protozoan parasite that infects intestinal epithelial cells and induces inflammation of the intestine. To better understand the inflammatory process occurring during cryptosporidiosis, we investigated in this study the kinetics of chemokine expression in the mucosa of mice by quantitative reverse transcription-PCR. Our results demonstrate that among the chemokine mRNAs studied, gamma interferon (IFN-)-inducible protein 10 (IP-10), monokine induced by IFN- (MIG), i-TAC, lymphotactin, macrophage inflammatory protein 1ß (MIP-1ß), and RANTES mRNAs were strongly up-regulated in infected neonate mice, which correlated with the immunofluorescence staining results showing T-cell and macrophage infiltration in the mucosa. Our in vitro data showed that intestinal epithelial cells infected by C. parvum or stimulated by the proinflammatory cytokines (IFN-, interleukin-1ß, and tumor necrosis factor alpha) produce a pattern of chemokine secretion similar to that observed in vivo, suggesting that these cells may take part in the initial production of chemokines. In order to identify the chemokines responsible for the recruitment of the inflammatory cells leading to a protective immune response, we compared the patterns of chemokine expression in a healing neonate mouse model and a nonhealing IFN- knockout (GKO) mouse model of cryptosporidiosis. In the absence of IFN-, the chemokine response was altered for IP-10, MIG, i-TAC, RANTES, and MIP-1ß mRNAs, while the three ELR C-X-C chemokine mRNAs studied (lipopolysaccharide-induced C-X-C chemokine, MIP-2, and KC mRNAs) were strongly overexpressed. These results are consistent with the neutrophil recruitment observed in the lamina propria of GKO mice at day 9 postinfection but are not consistent with the hypothesis that these cells play an important role in the resolution of the infection. On the contrary, the altered response of chemokines responsible for the recruitment of macrophages and T cells in GKO mice suggests that these two populations may be critical in the development of a protective immune response.

Editor: J. M. Mansfield

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