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Complement receptor 3 deficiency influences lesion progression during Leishmania major infection in BALB/c mice
Cristina R Carter1, James P Whitcomb, Jessica A Campbell
1Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana 46556, USA.
Abstract:
Leishmania major is an obligately intracellular protozoan parasite that causes cutaneous leishmaniasis. Like numerous intracellular pathogens, Leishmania exploits cell surface receptors as a means of entry into host cells. Complement receptor 3 (CR3; also called CD11b/CD18), a beta(2) integrin on phagocytic cells, is one such receptor. Ligation of CR3 has been shown to inhibit the production of interleukin-12, the cytokine that is pivotal in establishing the cell-mediated response necessary to combat intracellular infection. Here we investigate the role that CR3 plays in the establishment and progression of cutaneous leishmaniaisis in vivo. Dermal lesions of wild-type BALB/c mice are characteristically progressive and lead to extensive tissue necrosis coupled with elevated parasite burdens; CD11b-deficient BALB/c mice, however, demonstrate an intermediate phenotype characterized by chronic lesions and a reduced incidence of tissue damage. Infection followed by a reinfection challenge indicates that both susceptible (BALB/c) and resistant (C57BL/6) mice, regardless of CD11b status, develop resistance to L. major. In addition, CD11b does not bias the T helper cytokine response to L. major infection. Our results further indicate that CD11b is not necessary for disease resolution in resistant mice; rather, this protein appears to play a minor role in susceptibility.
Insights
Complement receptor 3 (CR3) plays a minor role in Leishmania major infection susceptibility. CD11b-deficient mice show reduced tissue damage, indicating CR3 is not essential for resolving cutaneous leishmaniasis.
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- Leishmania major causes cutaneous leishmaniasis by entering host cells.
- Complement receptor 3 (CR3), a beta(2) integrin, facilitates pathogen entry and can suppress interleukin-12 production.
- CR3's role in vivo during Leishmania major infection is not fully understood.
Purpose of the Study:
- To investigate the in vivo role of CR3 (CD11b) in the establishment and progression of cutaneous leishmaniasis.
- To determine if CR3 influences host resistance or susceptibility to Leishmania major infection.
Main Methods:
- Comparison of lesion development and parasite burden in wild-type versus CD11b-deficient BALB/c mice infected with Leishmania major.
- Assessment of host resistance following reinfection challenge in both susceptible (BALB/c) and resistant (C57BL/6) mouse strains, with and without CD11b.
- Analysis of T helper cytokine responses in relation to CD11b status during Leishmania major infection.
Main Results:
- CD11b-deficient mice exhibited an intermediate phenotype with chronic lesions and reduced tissue damage compared to wild-type mice.
- Both susceptible and resistant mouse strains developed resistance to Leishmania major upon reinfection, irrespective of CD11b status.
- CD11b deficiency did not alter the T helper cytokine response to Leishmania major infection.
Conclusions:
- CD11b plays a minor role in Leishmania major susceptibility.
- CD11b is not necessary for disease resolution in resistant mice.
- CR3 (CD11b) is not a critical factor in determining the overall T helper cytokine response or acquired resistance to Leishmania major.
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