PMID- 11179287
OWN - NLM
STAT- MEDLINE
DCOM- 20010524
LR  - 20181113
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 69
IP  - 3
DP  - 2001 Mar
TI  - Expression of chemokine genes in human dermal microvascular endothelial cell 
      lines infected with Orientia tsutsugamushi.
PG  - 1265-72
AB  - Scrub typhus, caused by Orientia tsutsugamushi, is characterized by local as well 
      as systemic inflammatory manifestations. The main pathologic change is focal or 
      disseminated multiorgan vasculitis, which is caused by the destruction of 
      endothelial cells and perivascular infiltration of leukocytes. We investigated 
      the regulation of chemokine induction in transformed human dermal microvascular 
      endothelial cells (HMEC-1) in response to O. tsutsugamushi infection. The 
      monocyte chemoattractant protein-1 (MCP-1) and interleukin 8 (IL-8) mRNAs were 
      induced, and their levels showed a transitory peak at 3 and 6 h, respectively. 
      The RANTES transcript was detected at 6 h after infection, with increased levels 
      evident by 48 h. The induction of the MCP-1 and IL-8 genes was not blocked by 
      cycloheximide, suggesting that de novo protein synthesis of host cell proteins is 
      not required for their transcriptional activation. Heat- or UV-inactivated O. 
      tsutsugamushi induced a similar extent of MCP-1 and IL-8 responses. The induction 
      of MCP-1 and IL-8 transcripts in the endothelial cells by O. tsutsugamushi was 
      not blocked by the inhibitors of NF-kappaB. Furthermore, the activation of 
      NF-kappaB was not detected in HMEC-1 stimulated with O. tsutsugamushi. These 
      results demonstrate that heat-stable molecules of O. tsutsugamushi induce the 
      MCP-1 and IL-8 genes and the induction of the chemokine genes may be mediated by 
      an NF-kappaB independent mechanism. We also showed that another major 
      transcription factor, activator protein-1 (AP-1), was up-regulated in HMEC-1 
      after O. tsutsugamushi infection. This suggests the possible involvement of AP-1 
      in the chemokine gene expression.
FAU - Cho, N H
AU  - Cho NH
AD  - Department of Microbiology and Immunology, Seoul National University College of 
      Medicine and Institute of Endemic Disease, Seoul National University Medical 
      Research Center, Seoul 110-799, Republic of Korea.
FAU - Seong, S Y
AU  - Seong SY
FAU - Choi, M S
AU  - Choi MS
FAU - Kim, I S
AU  - Kim IS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-8)
RN  - 0 (NF-kappa B)
RN  - 0 (Thiocarbamates)
RN  - 0 (Transcription Factor AP-1)
RN  - 135467-92-4 (prolinedithiocarbamate)
RN  - 402-71-1 (Tosylphenylalanyl Chloromethyl Ketone)
RN  - 9DLQ4CIU6V (Proline)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CCL2/biosynthesis
MH  - Chemokines/*biosynthesis/genetics
MH  - Dermis/blood supply/cytology/*metabolism/microbiology
MH  - Endothelium, Vascular/cytology/*metabolism/microbiology
MH  - Gene Expression Regulation
MH  - Inflammation Mediators/*metabolism
MH  - Interleukin-8/biosynthesis
MH  - NF-kappa B/metabolism
MH  - Orientia tsutsugamushi/*pathogenicity
MH  - Proline/analogs & derivatives/pharmacology
MH  - Thiocarbamates/pharmacology
MH  - Tosylphenylalanyl Chloromethyl Ketone/pharmacology
MH  - Transcription Factor AP-1/metabolism
PMC - PMC98016
EDAT- 2001/02/17 11:00
MHDA- 2001/05/26 10:01
PMCR- 2001/03/01
CRDT- 2001/02/17 11:00
PHST- 2001/02/17 11:00 [pubmed]
PHST- 2001/05/26 10:01 [medline]
PHST- 2001/02/17 11:00 [entrez]
PHST- 2001/03/01 00:00 [pmc-release]
AID - 0772 [pii]
AID - 10.1128/IAI.69.3.1265-1272.2001 [doi]
PST - ppublish
SO  - Infect Immun. 2001 Mar;69(3):1265-72. doi: 10.1128/IAI.69.3.1265-1272.2001.