CD2 deficiency partially prevents small bowel inflammation and improves parasite control in murine Toxoplasma gondii infection

doi:10.3748/wjg.v13.i31.4207

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Aug 21, 2007 (publication date) through Nov 5, 2024

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Basic Research

World J Gastroenterol. Aug 21, 2007; 13(31): 4207-4213
Published online Aug 21, 2007. doi: 10.3748/wjg.v13.i31.4207

CD2 deficiency partially prevents small bowel inflammation and improves parasite control in murine Toxoplasma gondii infection

Nina N Pawlowski, Daniela Struck, Katja Grollich, Anja A Kühl, Martin Zeitz, Oliver Liesenfeld, Jörg C Hoffmann

Nina N Pawlowski, Katja Grollich, Anja A Kühl, Martin Zeitz, Jörg C Hoffmann, Medizinische Klinik I, Charité- Universitätsmedizin Berlin, Campus Benjamin Franklin, D12200 Berlin, Germany

Daniela Struck, Oliver Liesenfeld, Institut für Mikrobiologie und Hygiene, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, D12203 Berlin, Germany

Author contributions: All authors contributed equally to the work.

Supported by the German Research Foundation (DFG), No. SFB633/B3 and 633/B6

Correspondence to: Jörg C Hoffmann, MD, Innere Medizin I, St. Marienkrankenhaus, Salzburger Straße 15, D67067 Ludwigshafen, Germany. joerg.hoffmann@charite.de

Telephone: +49-30-84453950 Fax: +49-30-84454481

Received: March 9, 2007
Revised: March 23, 2007
Accepted: March 31, 2007
Published online: August 21, 2007

Abstract

AIM: To investigate whether bowel inflammation and/or parasite control is altered in the absence of the T cell adhesion molecule CD2.

METHODS: Wildtype (WT) and CD2 deficient (CD2^-/-) mice were infected with 100 cysts of Toxoplasma gondii (T. gondii) (ME49) by gavage. On d 7 after infection mice were killed. Necrosis and the number of parasites/cm ileum were determined. Cytokine levels of stimulated cells as well as sera were evaluated. Secondly, survival of WT vs CD2^-/- mice was analysed using Kaplan-Meier analysis.

RESULTS: CD2^-/- mice survived longer than WT mice (mean: 23.5 vs 7.1 d, P = 0.001). Further, CD2^-/- mice showed less weight loss and less ileal inflammation than WT mice at d 7 post infection. In addition, the number of parasites in the ileum was significantly lower in CD2^-/- mice than in WT mice (88 ± 12 vs 349 ± 58 cm, P < 0.01). This was paralleled by lower production of IFN-γ and IL-6 from TLA-stimulated mLN cells and increased IFN-γ production by splenocytes.

CONCLUSION: CD2 deficient mice are more resistant to T. gondii infection than WT mice. In contrast to most current immunosuppressive or biological therapies CD2 deficiency reduces intestinal inflammation and at the same time helps to control infection.

Keywords: CD2; IL-6; Ileitis; Inflammatory bowel disease; Interferon-γ; Toxoplasma gondii