Granulocytic ehrlichiosis in mice deficient in phagocyte oxidase or inducible nitric oxide synthase

Abstract

Mice deficient in phox (gp91(phox-/-)) or NOS2 (NOS2(-/-)) were infected with the agent of human granulocytic ehrlichiosis (HGE) to evaluate the importance of these pathways in the eradication of HGE bacteria. NOS2(-/-) mice had delayed clearance of the HGE agent in comparison to control or gp91(phox-/-) mice, suggesting that reactive nitrogen intermediates play a role in the early control of HGE.

FIG. 1

HGE infection in gp91^phox−/− mice. At 8 and 12 days, splenocytes from HGE-infected gp91^phox−/− and control mice (five animals per group) were isolated and pooled, and RT-PCR was performed using HGE-specific primers. One of three studies with similar results is shown.

FIG. 2

HGE infection in NOS2^−/− and control mice. At 8, 12, and 20 days, RT-PCR analysis using HGE specific primers was performed. Five mice were used in each group. One of four experiments with similar results is shown.

FIG. 3

Effect of HGE infection on NOS2 levels in IFN-γR^−/− mice. At 12 days splenocytes were analyzed for HGE bacteria and NOS2 induction by RT-PCR. One of three studies with similar results is shown.