Persistent Chlamydia trachomatis Infection of HeLa Cells Mediates Apoptosis Resistance through a Chlamydia Protease-Like Activity Factor-Independent Mechanism and Induces High Mobility Group Box 1 Release

• DOI: 10.1128/iai.05619-11
• Publication Date: 2011-10-25T02:21:28Z
• Authors: Jürgen Rödel; Christina Große; Hangxing Yu; Katharina Wolf; Gordon P. Otto; Elisabeth Liebler...; Vera Forsbach-Birk; Eberhard Straube
• Keywords: Proinflammatory cytokine; Chlamydiae; Staurosporine; HeLa; Inhibitor of apoptosis

Intracellular persistence of Chlamydia trachomatis has been implicated in the development chronic infection that can result pelvic inflammatory disease and tubal sterility. By inhibition host cell apoptosis, chlamydiae have evolved a strategy to maintain intracellular environment for replication persistence. Both antiapoptotic cell-derived factors chlamydial protease-like activity factor (CPAF) are involved Chlamydia-mediated apoptosis resistance. Here, we show HeLa cells infected with gamma interferon (IFN-γ)-induced persistent C. serovar D, expression CPAF is downregulated, proapoptotic protease substrates not cleaved. Persistent protected from when they were exposed staurosporine. Small-interfering RNA-mediated myeloid leukemia 1 (Mcl-1) protein upregulation sensitized persistently apoptosis. The inhibitor 2 (IAP-2) seems be relevant this context because IAP-2 was induced response IFN-γ treatment. Although inhibited, caused membrane disintegration, as measured by increased release cytokeratin 18 cells. Moreover, released significantly amounts high mobility group box (HMGB1) which represents proinflammatory damage-associated pattern molecule. data study suggest independently but may promote inflammation through HMGB1 release.