
@Article{ecn.2006.0041,
AUTHOR = {Soraya Meghari, Benoît Desnues, Christian Capo, Georges E. Grau, Didier Raoult, Jean-Louis Mege},
TITLE = {<i>Coxiella burnetii</i> stimulates production of RANTES and MCP-1 by mononuclear cells: modulation by adhesion to endothelial cells and its implication in Q fever},
JOURNAL = {European Cytokine Network},
VOLUME = {17},
YEAR = {2006},
NUMBER = {4},
PAGES = {253--259},
URL = {http://www.techscience.com/ECN/v17n4/66136},
ISSN = {1952-4005},
ABSTRACT = {Q fever is an infectious disease caused by <i>Coxiella burnetii</i>, which may become chronic when
cytokine network and cell-mediated immune responses are altered. Chemokines, such as Regulated upon
Activation, Normal T cell Expressed and Secreted (RANTES, CCL5) and Monocyte Chemoattractant Protein-1
(MCP-1, CCL2), are specialized in the trafficing of peripheral blood mononuclear cells (PBMC), and are
associated with T cell polarization that is essential for intracellular survival of <i>C. burnetii</i>. The present study
investigated whether or not the infection status (no infection and acute or chronic infection with <i>C. burnetii</i>) of
donors, affected the production of the two chemokines by PBMC with or without stimulation with virulent and
avirulent <i>C. burnetii</i>. Our ﬁndings indicate that in vitro exposure to virulent or avirulent <i>C. burnetii</i> stimulated the
production of RANTES and MCP-1 in PBMC obtained from healthy adults. The co-cultivation of endothelial cells
and human PBMC resulted in an increased production of MCP-1 and the up-regulation of RANTES, which were
contact-dependent. Unstimulated PBMC from patients with acute or chronic Q fever overproduced MCP-1.
Interestingly, the addition of <i>C. burnetii</i> resulted in an increased production of RANTES and MCP-1 by PBMC
obtained from patients with chronic Q fever, and the co-cultivation of PBMC with endothelial cells ampliﬁed
increased production of chemokines. Circulating levels of RANTES and MCP-1 were also increased in chronic Q
fever. We suggest that the overproduction of RANTES and MCP-1 secondary to the contact of PBMC with
endothelium may perpetuate exaggerated inﬂammatory responses leading to inappropriate PBMC trafficking and
to the pathogenesis of Q fever.},
DOI = {10.1684/ecn.2006.0041}
}



