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Chlamydia trachomatis (CT) as well as Chlamydophila pneumoniae (CP) cause chronic inflammatory diseases in humans. Persistently infected monocytes are involved in the pathogenesis by inducing mediators of inflammation.An in vitro system of chlamydial persistence in human peripheral blood monocytes (HPBM) was used to investigate prostaglandin E2 (PGE2) production and the expression of the key enzyme for prostaglandin production, cyclooxygenase-2 (COX-2). PGE2 production was determined by PGE2-ELISA of HPBM-culture supernatants. Cox-2 mRNA expression was measured by real-time RT-PCR of total RNA isolated from HPBM.Both, CT and CP, stimulated PGE2 production of HPBM in vitro. Equivalent numbers of CT per host cell induced a higher PGE2-response compared to CP. The amount of synthesized PGE2 depended on the chlamydial multiplicity of infection (MOI). Even at an MOI of 10 the amount of CT- and CP-induced prostaglandin, respectively, was lower than the amount of prostaglandin induced by E. coli lipopolysaccharide (LPS) at a concentration of 10μg/ml. In contrast to stimulation with LPS, Chlamydia-induced PGE2 production as well as cox-2 mRNA decreased after day 1 post infection (p.i.). These data indicate that Chlamydia stimulate PGE2 production in human monocytes.Since Chlamydia are often contaminated by mycoplasma, the influence of mycoplasma on the prostaglandin production was investigated additionally. Mycoplasma fermentans (MF) also stimulated PGE2 production. The co-infection of mycoplasma and Chlamydia resulted in an additive effect in the production of PGE2. Thus it is important to use host cells and Chlamydia free of mycoplasma contamination for the analysis of Chlamydia-induced prostaglandin production. [Copyright &y& Elsevier]