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-Mediated Control of Coxiella burnetii Survival in Monocytes: The Role of Cell Apoptosis and TNF1
Unité des Rickettsies, Université de la Méditerranée, Centre National de la Recherche Scientifique, Faculté de Médecine, Marseille, France
The treatment of infectious diseases caused by intracellular
bacteria, such as Q fever, may benefit from cytokines acting on
macrophages. Monocytic THP-1 cells were infected with Coxiella
burnetii, the etiological agent of Q fever, and then treated
with IFN-
. While C. burnetii multiplied in untreated
monocytes, IFN- reduced bacterial viability after 24 h of
treatment and reached maximum inhibition after 96 h. IFN- also
affected the viability of infected cells. Cell death resulted from
apoptosis; occurring 24 h after the addition of IFN-, it
reached a maximum after 48 h and was followed by necrosis.
Reactive oxygen intermediates were not required for C.
burnetii killing, since monocytes from patients with chronic
granulomatous disease were microbicidal in response to IFN-. The
role of cytokines was also investigated. IFN- elicited a moderate
release of IL-1ß in infected monocytes. Moreover, the IL-1 receptor
antagonist did not affect C. burnetii survival,
suggesting that IL-1ß was not involved in the bacterial killing
induced by IFN-. TNF was involved in IFN--induced killing of
C. burnetii and cell death. IFN- induced mRNA
expression and sustained secretion of TNF. Neutralizing Abs to TNF as
well as Abs directed against TNF receptors I and II,
significantly prevented IFN--dependent killing of C.
burnetii and cell death. These results suggest that IFN-
promotes the killing of C. burnetii in monocytes through
an apoptotic mechanism mediated in part by TNF.
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