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Clinical and Diagnostic Laboratory Immunology, January 2000, p. 6-8, Vol. 7, No. 1
Department of Pathology, The Johns Hopkins
Medical Institutions,1 and Department of
Pathology, University of Maryland School of
Medicine,2 Baltimore, Maryland; St.
Mary's-Duluth Clinic Medical Center, Duluth,
Minnesota3; and Department of
Pathology4 and Division of Infectious
Diseases, Department of Medicine,5 New York
Medical College, Valhalla, New York
Received 2 July 1999/Returned for modification 18 August
1999/Accepted 22 September 1999
Human granulocytic ehrlichiosis (HGE) is caused by obligate
intracellular bacteria in the Ehrlichia phagocytophila
group. The disease ranges from subclinical to fatal. We speculated that cell-mediated immunity would be important for recovery from and potentially in the clinical manifestations of HGE; thus, serum tumor
necrosis factor alpha (TNF-
1071-412X/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Serum Cytokine Responses during Acute Human Granulocytic
Ehrlichiosis
), interleukin 1
(IL-1
), gamma interferon (IFN-
), IL-10, and IL-4 concentrations were studied. IFN-
(1,035 ± 235 pg/ml [mean ± standard error of the
mean]) and IL-10 (118 ± 46 pg/ml) concentrations were
elevated in acute-phase sera versus convalescent sera and normal
subjects (P
0.013 and P
0.018,
respectively). TNF-
, IL-1
, and IL-4 levels were not elevated.
Cytokine levels in severely and mildly affected patients were not
different. HGE leads to induction of IFN-
-dominated cell-mediated
immunity associated with clinical manifestations, recovery from
infection, or both.
*
Corresponding author. Mailing address: Division of
Medical Microbiology, Department of Pathology, The Johns Hopkins
Medical Institutions, Meyer B1-193, 600 N. Wolfe St., Baltimore, MD
21287. Phone: (410) 955-5077. Fax: (410) 614-8087. E-mail:
sdumler{at}jhmi.edu.
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