Int J Infect Dis 1999; 4:46-50

Objectives: Chlamydiae are obligate intracellular pathogens that cause many diseases for which the pathogenic mechanisms are largely unknown. Because reactive oxygen species (ROS) have been implicated in pathogenesis of many viral and bacterial infections, the authors assessed the release of ROS in selected host cells (monocytes, Sup-T1 cells, and Hep-2 cells) infected with Chlamydia trachomatis. Methods: Infected cell cultures demonstrated a dramatic depletion of uric acid from culture media that was not seen in uninfected cultures. Reactive oxygen species generated in infected cultures were associated with the formation of lipid peroxides in host cell membrane. Results: There was a significant increase in lipid peroxide levels in infected cells compared to uninfected controls. Ascorbic acid treatment of infected cell cultures reduced the formation of membrane lipid peroxides. Conclusions: These results suggest that ROS produced during chlamydial replication cause membrane lipid peroxidation. The role of ROS-induced membrane damage in chlamydial pathogenesis is discussed.

KEYWORDS: ascorbic acid, Chlamydia trachomatis replication, membrane lipid peroxidation, ROS

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