| Autor: |
Rödel, J., Groh, Annemarie, Hartmann, Matthias, Schmidt, Karl-Hermann, Lehmann, Marc, Lungershausen, Wolfgang, Straube, Eberhard |
| Zdroj: |
Medical Microbiology & Immunology; May1999, Vol. 187 Issue 4, p205-212, 8p |
| Abstrakt: |
Synovial fibroblasts probably represent host cells for Chlamydia trachomatis during initial intra-articular infection in reactive arthritis. In vitro synovial cells produce interferon- β (IFN- β) in response to chlamydial infection. IFN- β expression can be activated by interferon regulatory factor-1 (IRF-1) and interferon-stimulated gene factor 3 γ (ISGF3 γ). In this study, we demonstrate that infection of synovial fibroblasts with C. trachomatis serotype D induced the expression of IRF-1 mRNA as shown by reverse transcription-PCR. Tumor necrosis factor- α (TNF- α) stimulation enhanced IRF-1 mRNA levels in infected cells and was required to detect IRF-1 protein by immunoblotting. The level of constitutively expressed IRF-2 was not significantly affected after infection. C. trachomatis was found to cause an up-regulation of ISGF3 γ protein in synovial cells. Induction of the tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase (IDO) is an important mechanism of the host cell response to control intracellular infection by chlamydiae. It has been described that IRF-1 can induce IDO gene expression. Infection of synovial fibroblasts alone in the absence of exogenous cytokine induced the expression of IDO mRNA which was enhanced by TNF- α treatment. The stimulation of IRF-1, ISGF3 γ, and IDO expression was most effective when viable chlamydiae were used as inoculum. Neutralization of IFN- β in the culture medium of infected cells diminished but did not abrogate expression of IRF-1, ISGF3 γ, and IDO. The increased production of IRF-1 and ISGF3 γ in C. trachomatis-infected synovial fibroblasts may contribute to induction of IFN- β and IDO. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
Full text from SpringerLink