Inhibition of growth of Chlamydia trachomatis by tumor necrosis factor is accompanied by increased prostaglandin synthesis

Development of Chlamydia trachomatis (L₂/434/Bu) in HEp-2 cells was inhibited by treatment of the cells with recombinant human alpha tumor necrosis factor (TFN). In the infected cultures that were treated with TNF, high concentrations of prostaglandins E₂ (PGE₂) were detected, exceeding by far the concentrations found in TNF-treated but uninfected cells or in infected cells that were not treated with TNF. PGE₂ levels increased gradually for 2 days after infection. Raising the tryptophan concentration in the culture medium, which reversed the inhibition of chlamydial replication by TNF, also blocked the increase in PGE₂ formation. However, neutralizing antibodies to beta interferon, which also interfered with the antichlamydial effect of TNF, did not decrease PGE₂ formation. Excessive formation of PGE₂ by cells infected with chlamydiae and treated by TNF might be related to some of the complications associated with chlamydial infection.