Effect of Sex onCoxiella burnetiiInfection: Protective Role of 17β‐Estradiol
Author(s) -
Marc Léone,
Amélie Honstettre,
Hubert Lépidi,
Christian Capo,
Françis Bayard,
Didier Raoult,
JeanLouis Mège
Publication year - 2004
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/380798
Subject(s) - coxiella burnetii , q fever , spleen , granuloma , immunology , biology , zoonosis , pathogenesis , wolbachia , rickettsiaceae , rickettsia , microbiology and biotechnology , bacteria , virus , genetics
Q fever is a zoonosis caused by Coxiella burnetii and recently has been recognized as a potential agent of bioterrorism. In Q fever, men are symptomatic more often than women, despite equal seroprevalence. We hypothesized that sex hormones play a role in the pathogenesis of C. burnetii infection. When C57/BL6 mice were injected with C. burnetii, bacteria load and granuloma numbers were lower in females than in males. Ovarectomized mice showed increased bacteria load in the spleen and the liver, similar to that found in males. The granuloma number was also increased in ovarectomized mice and reached the levels found in males. Tissue infection and granulomatous response are largely under the control of estrogens: treatment of ovarectomized mice with 17beta-estradiol reduced both bacteria loads and granuloma numbers. These results show that sex hormones control host response to C. burnetii infection and may account for host-dependent clinical presentation of Q fever.
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