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Infection and Immunity, July 2000, p. 4361-4362, Vol. 68, No. 7
Section of Rheumatology, Department of
Internal Medicine, Yale University School of Medicine, New Haven,
Connecticut 06520
Received 22 February 2000/Returned for modification 24 March
2000/Accepted 28 March 2000
Mice deficient in phox (gp91phox
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Granulocytic Ehrlichiosis in Mice Deficient in
Phagocyte Oxidase or Inducible Nitric Oxide Synthase
/
) 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
gp91phox
/
mice, suggesting that reactive nitrogen
intermediates play a role in the early control of HGE.
*
Corresponding author. Mailing address: 608 Laboratory of Clinical Investigation, Section of Rheumatology,
Department of Internal Medicine, Yale University School of Medicine,
333 Cedar St., P.O. Box 208031, New Haven, CT 06520-8031. Phone: (203)
785-2453. Fax: (203) 785-7053. E-mail:
erol.fikrig{at}yale.edu.
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