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Infection and Immunity, March 2006, p. 1800-1808, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1800-1808.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Role for the CD28 Molecule in the Control of Coxiella burnetii Infection

Amélie Honstettre,1 Soraya Meghari,1 Jacques A. Nunès,2 Hubert Lepidi,1 Didier Raoult,1 Daniel Olive,2 and Jean-Louis Mege1*

Unité des Rickettsies, CNRS UMR 6020, Université de la Méditerranée, Faculté de Médecine, 13385 Marseille Cedex 5,1 Institut de Cancérologie de Marseille, INSERM UMR 599, Institut Paoli-Calmettes, 13009 Marseille Cedex, France2

Received 21 April 2005/ Returned for modification 9 June 2005/ Accepted 27 November 2005

Q fever is an infectious disease caused by Coxiella burnetii, an obligate intracellular bacterium that replicates in macrophages. As cell-mediated immune response to microbial pathogens requires signals mediated by T-cell receptors and costimulatory molecules such as CD28, we wondered if CD28 is involved in protection against C. burnetii infection. CD28-deficient (CD28–/–) mice were inoculated with C. burnetii by intraperitoneal and intravenous routes. With both wild-type and CD28–/– mice, C. burnetii organisms were detected exclusively in spleen and liver. The antibody response against C. burnetii was impaired in CD28–/– animals, but, surprisingly, the lack of CD28 decreased C. burnetii burden in the infected tissues, whatever the manner of inoculation of bacteria. The CD28 deficiency had no effect on either granuloma formation, which reflects cell-mediated immunity against C. burnetii, or the production of gamma interferon and tumor necrosis factor, two cytokines known to be involved in granuloma formation. On the other hand, the production of interleukin-10 (IL-10) by peritoneal macrophages was highly impaired in CD28–/– mice. The results suggest that CD28 initiates a signal that favors C. burnetii replication through the modulation of the IL-10 pathway.

* Corresponding author. Mailing address: Unité des Rickettsies, Université de la Méditerranée, Faculté de Médecine, 27 Blvd. J. Moulin, 13385 Marseille Cedex 5, France. Phone: (33) 4 91 32 43 75. Fax: (33) 4 91 38 77 72. E-mail: Jean-Louis.Mege{at}medecine.univ-mrs.fr.

Editor: J. L. Flynn

Infection and Immunity, March 2006, p. 1800-1808, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1800-1808.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Marmion, B.P., Sukocheva, O., Storm, P.A., Lockhart, M., Turra, M., Kok, T., Ayres, J., Routledge, H., Graves, S. (2009). Q fever: persistence of antigenic non-viable cell residues of Coxiella burnetii in the host--implications for post Q fever infection fatigue syndrome and other chronic sequelae. QJM 102: 673-684 [Abstract] [Full Text]  


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