Abstract
BackgroundAn increasing number of studies suggest that chlamydiae can infect immune cells. The altered immune cell function could contribute to the progression of several chronic inflammatory diseases.The aim of this study was to comparatively evaluate Chlamydia pneumoniae (CP) and Chlamydia trachomatis (CT) interactions with in vitro infected human blood monocytes.ResultsFresh isolated monocytes were infected with viable CP and CT elementary bodies and infectivity was evaluated by recultivating disrupted monocytes in permissive epithelial cells.The production of reactive oxygen and nitrogen species was studied in the presence of specific fluorescent probes. Moreover, TNF-α, INF-α, INF-β and INF-γ gene expression was determined.CT clearance from monocytes was complete at any time points after infection, while CP was able to survive up to 48 hours after infection. When NADPH oxydase or nitric oxide synthase inhibitors were used, CT infectivity in monocytes was restored, even if at low level, and CT recovery’s rate was comparable to CP one.CT-infected monocytes produced significantly higher levels of reactive species compared with CP-infected monocytes, at very early time points after infection. In the same meanwhile, TNF-α and INF-γ gene expression was significantly increased in CT-infected monocytes.ConclusionsOur data confirm that CP, but not CT, is able to survive in infected monocytes up to 48 hours post-infection. The delay in reactive species and cytokines production by CP-infected monocytes seems to be crucial for CP survival.
Highlights
An increasing number of studies suggest that chlamydiae can infect immune cells
Azenabor and his collaborators [17] showed that macrophages infected by C. pneumoniae (CP) produced reactive oxygen species (ROS) through membrane-associated NADPH oxidase with oxidative phosphorylation levels depending on Ca2+ influx signals
It is noteworthy to underline that all the results obtained by this group derived from their infection data on THP-1 cell line rather than primary cells, such as freshly isolated human monocytes or animal peritoneum-derived macrophages. These findings show that chlamydial replication in monocytes/macrophages is limited and that infection of immune cells results in the secretion of a range of cytokines, production of reactive species, resistance to apoptosis and alteration of different macrophage functions
Summary
An increasing number of studies suggest that chlamydiae can infect immune cells. An increasing number of in vitro studies suggest that both CT and CP can be isolated from human peripheral blood and can infect immune cells, at least at a low level, [5,6]. An increase in ROS production or a decrease in antioxidant defenses leads to an imbalance of the redox state, which can result in apoptosis [16]. Azenabor and his collaborators [17] showed that macrophages infected by CP produced ROS through membrane-associated NADPH oxidase with oxidative phosphorylation levels depending on Ca2+ influx signals
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