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Aggravated Lyme carditis in CD11a-/- and CD11c-/- mice.
Mireia Guerau-de-Arellano1, Joseph Alroy, Daniel Bullard
1Department of Pathology, Tufts University School of Medicine, Jaharis 512, 150 Harrison Ave., Boston, MA 02111, USA.
Infection and Immunity
|October 22, 2005
Summary
Mice lacking CD18, a common beta2 integrin chain, show worsened Lyme carditis due to increased macrophages and MCP-1. Specific deficiencies in CD11a or CD11c integrins also exacerbate Lyme carditis, suggesting distinct roles in disease severity.
Area of Science:
- Immunology
- Microbiology
- Cardiovascular Science
Background:
- Lyme carditis, caused by Borrelia burgdorferi, is exacerbated in CD18 hypomorph mice.
- CD18 is essential for beta2 integrins like LFA-1 (CD11a/CD18), Mac-1 (CD11b/CD18), and p150,95 (CD11c/CD18).
- Increased macrophage infiltration and MCP-1 expression are hallmarks of aggravated Lyme carditis in CD18 hypomorph mice.
Purpose of the Study:
- To investigate the specific roles of beta2 integrins (CD11a, CD11b, CD11c) in the development of Lyme carditis.
- To elucidate the mechanisms underlying aggravated Lyme carditis in CD18-deficient models.
Main Methods:
- Analysis of Lyme carditis severity in CD11a-/-, CD11b-/-, and CD11c-/- mice infected with Borrelia burgdorferi.
- In vitro assessment of MCP-1 secretion by bone marrow-derived dendritic cells.
- In vivo measurement of MCP-1 mRNA expression in infected heart tissue.
Main Results:
- CD11a-/- and CD11c-/- mice, but not CD11b-/- mice, exhibited aggravated Lyme carditis.
- CD11c-/- mice showed elevated MCP-1 levels, similar to CD18 hypomorph mice.
- CD11a deficiency correlated with a higher Borrelia burgdorferi burden in the heart.
Conclusions:
- Deficiency in CD11a or CD11c integrins contributes to the aggravated Lyme carditis observed in CD18 hypomorph mice.
- These integrins may influence Lyme carditis severity through distinct mechanisms, potentially involving MCP-1 regulation and bacterial burden.