Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 181, Issue 1, Pages 374-378Publisher
UNIV CHICAGO PRESS
DOI: 10.1086/315206
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI041213] Funding Source: NIH RePORTER
- NIAID NIH HHS [R01 AI 41213-01] Funding Source: Medline
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Human granulocytic ehrlichiosis (HGE) results in fever, pancytopenia, and mild liver injury, We used a mouse model to examine immunity in the pathogenesis of HGE, HGE agent-infected C3H/HeJ mice were necropsied over 21 days. Histologic, immunohistologic, and serologic analyses, blood culture, tissue and blood polymerase chain reaction (PCR), cell counts, serum chemistries, and plasma cytokine ELISAs were performed, No clinical signs were detected. Ehrlichiae were identified in neutrophils in hematopoietic tissues maximally on day 7, Interleukin (IL)-10 levels were high throughout, whereas interferon (IFN)-gamma levels peaked on days 7 and 10 and dropped thereafter. Hepatic lymphohistiocytic aggregates with apoptoses were maximal at day 14, HGE-agent infection of mice induces pathologic changes similar to those in infected humans, despite differences in cytokine profile. The IFN-gamma peak prior to maximal pathologic change, when ehrlichiae are absent in tissues, suggests a role for host immunity in the pathogenesis of HGE.
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