PMID- 10858246
OWN - NLM
STAT- MEDLINE
DCOM- 20000720
LR  - 20210526
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 68
IP  - 7
DP  - 2000 Jul
TI  - Requirement for NF-kappaB in transcriptional activation of monocyte chemotactic 
      protein 1 by Chlamydia pneumoniae in human endothelial cells.
PG  - 4282-8
AB  - Infection with Chlamydia pneumoniae, a causative agent of acute and chronic 
      respiratory diseases, has recently been implicated as a potential risk factor in 
      atherosclerosis. Atherosclerotic lesions are characterized by monocyte 
      infiltration, which may be regulated by the chemokine monocyte chemotactic 
      protein 1 (MCP-1). We have previously shown that C. pneumoniae infection 
      stimulates MCP-1 production in human endothelial cells, an event which may be 
      specific to this species of Chlamydia, since Chlamydia trachomatis infection 
      fails to induce this response. To examine the underlying mechanisms by which C. 
      pneumoniae infection induces MCP-1 production in endothelial cells, the present 
      study investigated the role of transcription factor NF-kappaB in MCP-1 mRNA 
      expression. Human umbilical vein endothelial cells (HUVEC) were infected with the 
      coronary isolate C. pneumoniae A-03 or with C. trachomatis L2, and MCP-1 mRNA 
      expression was assessed after different periods of infection by reverse 
      transcription-PCR. Expression of MCP-1 mRNA in C. pneumoniae-infected HUVEC was 
      significantly elevated as early as 1 h postinfection and increased dramatically 
      by 12 and 24 h compared to baseline controls. Nuclear translocation of NF-kappaB 
      occurred by 30 min of infection, as determined by electrophoretic mobility shift 
      assays and immunofluorescence staining. Treatment of C. pneumoniae-infected HUVEC 
      with parthenolide, a specific inhibitor of NF-kappaB activation, suppressed MCP-1 
      mRNA expression. In contrast, infection with C. trachomatis L2 did not induce 
      MCP-1 mRNA in infected HUVEC and failed to activate NF-kappaB. Results from this 
      study demonstrate a requirement for NF-kappaB activation in stimulation of MCP-1 
      gene expression by C. pneumoniae in human endothelial cells. Furthermore, the 
      data suggest that, within the genus Chlamydia, functionally distinct signaling 
      pathways leading to NF-kappaB activation are utilized by C. pneumoniae in 
      endothelial cells during infection.
FAU - Molestina, R E
AU  - Molestina RE
AD  - Division of Infectious Diseases, Department of Medicine, University of Louisville 
      School of Medicine, Louisville, Kentucky 40292, USA.
FAU - Miller, R D
AU  - Miller RD
FAU - Lentsch, A B
AU  - Lentsch AB
FAU - Ramirez, J A
AU  - Ramirez JA
FAU - Summersgill, J T
AU  - Summersgill JT
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Chemokine CCL2)
RN  - 0 (DNA Primers)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Sesquiterpenes)
RN  - 2RDB26I5ZB (parthenolide)
SB  - IM
MH  - Arteriosclerosis/etiology
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Chemokine CCL2/*genetics
MH  - Chlamydia trachomatis/immunology/pathogenicity
MH  - Chlamydophila pneumoniae/immunology/*pathogenicity
MH  - DNA Primers/genetics
MH  - Endothelium, Vascular/*immunology/*microbiology
MH  - Humans
MH  - NF-kappa B/antagonists & inhibitors/*metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Sesquiterpenes/pharmacology
MH  - Signal Transduction
MH  - Transcriptional Activation
PMC - PMC101745
EDAT- 2000/06/17 09:00
MHDA- 2000/07/25 11:00
PMCR- 2000/07/01
CRDT- 2000/06/17 09:00
PHST- 2000/06/17 09:00 [pubmed]
PHST- 2000/07/25 11:00 [medline]
PHST- 2000/06/17 09:00 [entrez]
PHST- 2000/07/01 00:00 [pmc-release]
AID - 1640 [pii]
AID - 10.1128/IAI.68.7.4282-4288.2000 [doi]
PST - ppublish
SO  - Infect Immun. 2000 Jul;68(7):4282-8. doi: 10.1128/IAI.68.7.4282-4288.2000.