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Persistence of Infection Contributes to Heterologous Protection against Ehrlichiosis
Author(s) -
Thirumalapura Nagaraja,
Crossley Emily,
Walker David H,
Ismail Nahed
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.858.12
Subject(s) - biology , heterologous , ehrlichia , immunology , immunity , ehrlichiosis , virology , doxycycline , ehrlichia chaffeensis , cd8 , immune system , microbiology and biotechnology , tick , biochemistry , gene , antibiotics
Human monocytotropic ehrlichiosis (HME) is an emerging life‐threatening tick‐transmitted disease caused by the obligately intracellular bacterium, Ehrlichia chaffeensis . HME is modeled in mice using Ehrlichia muris , which causes persistent infection, and Ixodes ovatus Ehrlichia (IOE), which is either acutely lethal or cleared depending on the dose and route. Primary sublethal IOE infection does not protect mice against secondary IOE challenge, but persistent E. muris infection confers heterologous immunity against IOE. The objective of this study is to determine the role of bacterial persistence in the maintenance of protective immunity against IOE. E. muris‐ infected mice were treated with doxycycline or left untreated and then challenged with an ordinarily lethal dose of IOE. The cytokine production profiles of splenic memory T cell subsets were assessed by flow cytometry. Doxycycline treatment affected neither the numbers of antigen‐specific, IFN‐γ‐producing CD4 + and CD8 + T cells nor the bacterial burden following IOE challenge. However, spleens from treated mice had fewer numbers of effector memory (CD44 high CD62L low ) CD8 + T cells and produced less TGF‐β1. Histology and TUNEL assay revealed greater numbers of inflammatory cells and more extensive apoptosis in the liver of treated mice following IOE challenge. These results suggest that the persistence of E. muris infection contributes to protective heterologous immunity, possibly by inducing the accumulation of regulatory cells at the sites of infection.