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Infection and Immunity, April 2007, p. 1619-1625, Vol. 75, No. 4
0019-9567/07/$08.00+0     doi:10.1128/IAI.01535-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Induction of Host Chemotactic Response by Encephalitozoon spp.{triangledown}

Jeffrey Fischer, Jeffrey West, Nnenaya Agochukwu, Colby Suire, and Hollie Hale-Donze*

Louisiana State University, 202 Life Sciences Building, Baton Rouge, Louisiana 70803

Received 22 September 2006/ Returned for modification 30 October 2006/ Accepted 5 December 2006

Microsporidians are a group of emerging pathogens typically associated with chronic diarrhea in immunocompromised individuals. The number of reports of infections with these organisms and the disseminated pathology is growing as diagnostic tools become more readily available. However, little is known about the innate immune response induced by and generated against these parasites. Using a coculture chemotaxis system, primary human macrophages were infected with Encephalitozoon cuniculi or Encephalitozoon intestinalis, and the recruitment of naïve monocytes was monitored. Encephalitozoon spp. induced an average threefold increase in migration of naïve cells 48 h postinfection, which corresponded to optimal infection of monocyte-derived-macrophages. A limited microarray analysis of infected macrophages revealed several chemokines involved in the inflammatory responses whose expression was upregulated, including CCL1, CCL2, CCL3, CCL4, CCL7, CCL15, CCL20, CXCL1, CXCL2, CXCL3, CXCL5, and CXCL8. The levels of 6 of 11 chemokines also present in the microarray were confirmed to be elevated by protein profiling. Kinetic studies confirmed that secreted CCL2, CCL3, and CCL4 were expressed as early as 6 h postinfection, with peak expression at 12 to 24 h and expression remaining until 48 h postinfection. Neutralization of these chemokines, specifically CCL4, significantly reduced the number of migrating cells in vitro, indicating their role in the induction of monocyte migration. This mechanism of recruitment not only supports the evidence that in vivo cellular infiltration occurs but also provides new hosts for the parasites, which escape macrophages by rupturing the host cell. To our knowledge, this is the first documentation that chemokine production is induced by microsporidian infections in human macrophages.

* Corresponding author. Mailing address: Department of Biological Sciences, Louisiana State University, 202 Life Sciences Building, Baton Rouge, LA 70803. Phone: (225) 578-8411. Fax: (225) 578-2597. E-mail: hhaled1{at}lsu.edu.

{triangledown} Published ahead of print on 18 December 2006.

Editor: W. A. Petri, Jr.

Infection and Immunity, April 2007, p. 1619-1625, Vol. 75, No. 4
0019-9567/07/$08.00+0     doi:10.1128/IAI.01535-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Fischer, J., Suire, C., Hale-Donze, H. (2008). Toll-Like Receptor 2 Recognition of the Microsporidia Encephalitozoon spp. Induces Nuclear Translocation of NF-{kappa}B and Subsequent Inflammatory Responses. Infect. Immun. 76: 4737-4744 [Abstract] [Full Text]  


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