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Aarti Gautam, Monica Embers, Saurabh Dixit, Shree Singh, Lisa Morici, Rajeev Gautam, Vida Dennis, Differential expression and regulation of inflammatory mediators in macrophages from Lyme disease-resistant C57BL/6J and disease-susceptible C3H/HeN mice (37.6), The Journal of Immunology, Volume 184, Issue Supplement_1, April 2010, Page 37.6, https://doi.org/10.4049/jimmunol.184.Supp.37.6
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Abstract
C3H/HeN (C3H) mice develop severe arthritis whereas; C57BL/6J (C57) mice develop mild arthritis after experimental infection with the Lyme disease spirochete Borrelia burgdorferi. We hypothesize that these host responses may depend on differences in the expression and regulation of inflammatory mediators induced by spirochetes during the early stage of Lyme disease. In the present study, bone marrow-derived macrophages from C3H and C57 mice were stimulated with live B. burgdorferi or with its lipoprotein outer surface protein A; supernatants were collected and subjected to proteome analysis using multiplex ELISA. Both stimulants induced significantly higher levels of IL-6, TNF-α, IFN-γ, KC, IL-9, MCP1/CCL2, IL-5, GM-CSF, and IL-12p70 in cells of C3H than in those of C57 mice. In contrast, MIP1α/CCL3, MIP1β/CCL4, RANTES/CCL5, IP-10/CXCL10, MIP2/CXCL2, IL-17, IL-1α, IL-1β, LIX/CXCL5, G-CSF, CXCL9/MIG and IL-10 levels were significantly greater in C57 than in C3H mice. Exogenous IL-10 abrogated the expression levels of inflammatory mediators. Neutralization of endogenous IL-10 resulted in enhanced production of mediators; the effect was more evident in C57 mice. Our data show differential expression and regulation of inflammatory mediators in B. burgdorferi-stimulated macrophages of C57 and C3H mice. The potent action of endogenous IL-10, especially in C57, suggests a key role played by IL-10 to abrogate inflammation during the early stage of Lyme disease in this mouse strain.
