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Parasite Immunol. 2000 Nov;22(11):581-8.

Coinfection with Borrelia burgdorferi and the agent of human granulocytic ehrlichiosis suppresses IL-2 and IFN gamma production and promotes an IL-4 response in C3H/HeJ mice.

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Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, PO Box 2087, Rampart Road, Foothills Campus, Fort Collins, CO 80522, USA.


Previously we demonstrated that Borrelia burgdorferi transmission by Ixodes scapularis suppressed IL-2 and IFN gamma production and promoted IL-4 production in mice. The present studies were conducted to determine whether coinfection with the human granulocytic ehrlichiosis (HE) agent would promote a Th2 cytokine response in mice. Transmission to the spleen of the agent of human granulocytic ehrlichiosis (aoHGE) and B. burgdorferi occurred 4 and 7 days, respectively, after tick infestation. Coinfection synergized to suppress splenic IL-2 production 7-14 days after tick infestion. Transmission of B. burgdorferi or aoHGE alone significantly decreased splenic IFN gamma 4-7 days after tick infestation, while coinfection suppressed IFN gamma production 7-14 days after tick infestation. Splenic IL-4 production was significantly increased 4 days after coinfection, and by day 10, aoHGE plus B. burgdorferi induced greater splenic IL-4 (57.2 pg/ml, 348% of control values) than either organism transmitted alone (aoHGE, 22.7 pg/ml, B. burgdorferi, 25.1 pg/ml). Coinfection enhanced expansion of splenic T cells, CD4+ lymphocytes and B cells while decreasing CD8+ T cells. These data demonstrate that aoHGE and B. burgdorferi, when cotransmitted, suppress a systemic IL-2 and IFN gamma response, while strongly promoting systemic IL-4 production in the susceptible host. The antigen(s) responsible for this polarization are unknown and will be the subject of future studies.

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