Lack of dendritic cell maturation following infection by Coxiella burnetii synthesizing different lipopolysaccharide chemotypes.
Coxiella burnetii is an obligate intracellular bacterium and the etiologic agent of the zoonotic disease Q fever. Symptomatic infection is normally characterized by flu-like symptoms; however, in some cases, a persistent infection can ensue that may reactivate months or years after initial exposure to cause chronic disease. The mechanisms by which this obligate parasite evades clearance by the host immune response during persistent infection are unknown. We have previously demonstrated that lipopolysaccharide (LPS) length is critical in determining the response of human dendritic cells (DC) to C. burnetii. Here, we investigated whether LPS chemotype affects DC maturation or activation. Immature human DC were infected with three virulent strains of C. burnetii (Nine Mile phase I, S, or Priscilla) that produce chemically distinct LPS molecules. None of these strains stimulated significant upregulation of cell surface markers of DC maturation. Moreover, these strains were equally deficient in inducing DC IL-12p70 production or p38 mitogen-activated protein kinase phosphorylation. Infection of DC by virulent C. burnetii without stimulating significant maturation or inflammatory cytokine production may be a mechanism of immune evasion that results in persistent infection of an otherwise immunocompetent host. Our data indicate that LPS chemotype is not a determinant of DC maturation or cytokine production in response to C. burnetii.