1. Infection of C57BL/10ScCr and C57BL/10ScNCr mice withLeishmania majorreveals a role for Toll-like receptor 4 in the control of parasite replication
- Author
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Pascale Kropf, N. Freudenberg, Marina A. Freudenberg, Manuel Modolell, Chris Galanos, Ines Müller, Shanti Herath, and Christoph Kalis
- Subjects
Immunology ,Leishmaniasis, Cutaneous ,Mice, Transgenic ,Receptors, Cell Surface ,Parasite load ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Immune system ,Cutaneous leishmaniasis ,medicine ,Animals ,Immunology and Allergy ,Leishmania major ,Skin ,030304 developmental biology ,0303 health sciences ,Toll-like receptor ,Membrane Glycoproteins ,Innate immune system ,biology ,Toll-Like Receptors ,Receptors, Interleukin-12 ,Receptors, Interleukin ,Cell Biology ,biology.organism_classification ,medicine.disease ,Leishmania ,3. Good health ,Toll-Like Receptor 4 ,TLR4 ,030215 immunology - Abstract
The innate immune system is essential for host defense; it senses the presence of potentially pathogenic-invading microorganisms, and the contribution of Toll-like receptors (TLRs) to this response is increasingly recognized. In the present study, we investigated the contribution of TLR4 to the course of cutaneous leishmaniasis in vivo. We used C57BL/10ScNCr (TLR40/0) and C57BL/10ScCr [TLR4/interleukin-12 (IL-12)Rβ20/0] mice and compared the course of Leishmania major infection, parasite load, cell recruitment, and cytokine profile with those of wild-type C57BL/10ScSn mice. Our results confirm the importance of IL-12 receptor-mediated signaling in resistance to L. major infections. Importantly, we show that the lack of TLR4 results in an increased permissiveness for parasite growth during the innate and adaptive phase of the immune response and in delayed healing of the cutaneous lesions. The use of the tlr4 transgenic mouse strain TCr5 demonstrated unequivocally that TLR4 contributes to the efficient control of Leishmania growth in vivo.
- Published
- 2004
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