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
Ns. Zeidner et al., 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, PARASITE IM, 22(11), 2000, pp. 581-588
Previously we demonstrated that Borrelia burgdorferi transmission by Ixodes
scapularis suppressed IL-2 and IFN gamma production and promoted IL-4 prod
uction in mice. The present studies wee conducted to determine whether coin
fection wit the human granulocytic ehrlichiosis (HE) agent would promote a
Th2 cytokine response in mice. Transmission to the spleen of the agent of h
uman agranulocytic ehrlichiosis (aoHGE) and B. burgdorferi occurred 4 and 7
days, respectively, after tick infestation. Coinfection synergized to supp
ress splenic IL-2 production 7-14 days after tick infestation. Transmission
of B. burgdorferi or aoHGE alone significantly decreased splenic IFN gamma
4-7 days after tick infestation, while coinfection suppressed IFN gamma pr
oduction 7-14 days after tick infestation. Splenic IL-4 production was sign
ificantly 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 value
s) that either organism transmitted alone (aoHGE, 22.7 pg/ml, B. burgdorfer
i, 25.1 pg/ml). Coinfection enhanced expansion of splenic T cells, CD4(+) l
ymphocytes and B cells while decreasing CD8(+) T cells. These data demonstr
ate that aoHGE and B. burgdorferi, when cotransmitted, suppress a systemic
IL-2 and IFN gamma response, while strongly promoting systemic IL-4 product
ion in the susceptible host. The antigen(s) responsible for this polarizati
on are unknown and will be the subject of future studies.