PMID- 10363677
OWN - NLM
STAT- MEDLINE
DCOM- 19990804
LR  - 20191024
IS  - 0300-8584 (Print)
IS  - 0300-8584 (Linking)
VI  - 187
IP  - 4
DP  - 1999 May
TI  - Expression of interferon regulatory factors and indoleamine 2,3-dioxygenase in 
      Chlamydia trachomatis-infected synovial fibroblasts.
PG  - 205-12
AB  - Synovial fibroblasts probably represent host cells for Chlamydia trachomatis 
      during initial intra-articular infection in reactive arthritis. In vitro synovial 
      cells produce interferon-beta (IFN-beta) in response to chlamydial infection. 
      IFN-beta expression can be activated by interferon regulatory factor-1 (IRF-1) 
      and interferon-stimulated gene factor 3gamma (ISGF3gamma). 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-alpha (TNF-alpha) 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 ISGF3gamma 
      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-alpha treatment. The stimulation of IRF-1, ISGF3gamma, 
      and IDO expression was most effective when viable chlamydiae were used as 
      inoculum. Neutralization of IFN-beta in the culture medium of infected cells 
      diminished but did not abrogate expression of IRF-1, ISGF3gamma, and IDO. The 
      increased production of IRF-1 and ISGF3gamma in C. trachomatis-infected synovial 
      fibroblasts may contribute to induction of IFN-beta and IDO.
FAU - Rodel, J
AU  - Rodel J
AD  - Institute of Medical Microbiology, Friedrich Schiller University of Jena, 
      Germany. Roedel@bach.med.uni-jena.de
FAU - Groh, A
AU  - Groh A
FAU - Hartmann, M
AU  - Hartmann M
FAU - Schmidt, K H
AU  - Schmidt KH
FAU - Lehmann, M
AU  - Lehmann M
FAU - Lungershausen, W
AU  - Lungershausen W
FAU - Straube, E
AU  - Straube E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Med Microbiol Immunol
JT  - Medical microbiology and immunology
JID - 0314524
RN  - 0 (Antibodies)
RN  - 0 (Bacterial Proteins)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (IRF1 protein, human)
RN  - 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase)
RN  - 0 (Interferon Regulatory Factor-1)
RN  - 0 (Phosphoproteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 77238-31-4 (Interferon-beta)
RN  - 8DUH1N11BX (Tryptophan)
RN  - EC 1.13.11.11 (Tryptophan Oxygenase)
SB  - IM
MH  - Antibodies/immunology
MH  - Bacterial Proteins/biosynthesis
MH  - Cells, Cultured
MH  - Chlamydia trachomatis/drug effects/*growth & development
MH  - DNA-Binding Proteins/*biosynthesis
MH  - Fibroblasts/metabolism/*microbiology
MH  - Humans
MH  - Immunoblotting
MH  - Indoleamine-Pyrrole 2,3,-Dioxygenase
MH  - Interferon Regulatory Factor-1
MH  - Interferon-beta/immunology/physiology
MH  - Phagocytosis
MH  - Phosphoproteins/*biosynthesis
MH  - RNA, Messenger/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Synovial Membrane/*cytology
MH  - Tryptophan/pharmacology
MH  - Tryptophan Oxygenase/*biosynthesis
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1999/06/11 00:00
MHDA- 1999/06/11 00:01
CRDT- 1999/06/11 00:00
PHST- 1999/06/11 00:00 [pubmed]
PHST- 1999/06/11 00:01 [medline]
PHST- 1999/06/11 00:00 [entrez]
AID - 10.1007/s004300050094 [doi]
PST - ppublish
SO  - Med Microbiol Immunol. 1999 May;187(4):205-12. doi: 10.1007/s004300050094.