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,§
Departments of
*
Dermatology and
Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104;
The Wistar Institute, Philadelphia, PA 10104; and
§
Department of Microbiology, Albert Szent-Gyorgyi Medical University, Szeged, Hungary
Chlamydia pneumoniae is a common
cause of pulmonary infection, with serum positivity in at least 50% of
the general population. In this study, we report that human PBMCs
exposed to C. pneumoniae are resistant to apoptosis
induced by the potent photoactivated chemotherapeutic agents
8-methoxypsoralen and hypericin. In contrast, PBMCs treated with a
heat-inactivated inoculum exhibit normal susceptibility to apoptosis.
We also observed that human PBMCs are responsive to C.
pneumoniae infection by secretion of key immune regulatory
cytokines, including IL-12 and IL-10. While IL-12 may play an important
role in limiting C. pneumoniae proliferation within
cells, IL-10 serves an anti-inflammatory function by
down-regulating proinflammatory cytokines such as IL-12 and TNF-
.
Depletion of endogenous IL-10, but not of IL-12, abolished the
apoptosis resistance of C. pneumoniae-infected
PBMCs. Furthermore, addition of exogenous IL-10, but not IL-12,
significantly increased the resistance of control inoculum-treated
PBMCs to photoactivated 8-methoxypsoralen- and hypericin-induced
apoptosis. Therefore, we conclude that C. pneumoniae
possesses an antiapoptotic mechanism. The resistance to apoptosis
observed in PBMCs exposed to C. pneumoniae is due, at
least partially, to the IL-10 induced during C.
pneumoniae infection.
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