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 (TNF). In the infected cultures that were treated with TNF, high concentrations of prostaglandin 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.
Holtmann
H
H
Department of Pharmacology and Toxicology, Medical School, Hannover, Federal Republic of Germany.
Shemer-Avni
Y
Y
Wessel
K
K
Sarov
I
I
Wallach
D
D
D002692:Chlamydia trachomatis / Q000187:drug effects* / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid; D015232:Dinoprostone / Q000096:biosynthesis*; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology; D009500:Neutralization Tests; D011994:Recombinant Proteins; D014364:Tryptophan / Q000494:pharmacology; D014407:Tumor Cells, Cultured; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D014364:Tryptophan; D015232:Dinoprostone