PMID- 10923243
OWN - NLM
STAT- MEDLINE
DCOM- 20001228
LR  - 20191025
IS  - 0190-2148 (Print)
IS  - 0190-2148 (Linking)
VI  - 26
IP  - 4
DP  - 2000 Jun
TI  - Asbestos exposure induces MCP-1 secretion by pleural mesothelial cells.
PG  - 241-55
AB  - We showed previously that both crocidolite and chrysotile asbestos inhalation 
      induced a persistent macrophage inflammatory response within the pleural space of 
      the rat. We postulated that the stimulus for pleural macrophage recruitment after 
      asbestos exposure was the induction of monocyte chemoattractant protein-1 (MCP-1) 
      synthesis by pleural mesothelial cells. To test this hypothesis, rat pleural 
      mesothelial cells (RPMC) were cultured with or without chrysotile or crocidolite 
      asbestos fibers (8 micrograms/cm2) in the presence (50 ng/mL) or absence of 
      either tumor necrosis factor-alpha (TNF-alpha) or interleukin-1 beta (IL-1 beta). 
      MCP-1 mRNA expression was assessed by RT-PCR in RPMC cultured for 2 to 24 hours, 
      and MCP-1 protein secretion was measured by ELISA in conditioned medium from 
      24-hour and 48-hour cultures. Crocidolite and chrysotile fibers induced MCP-1 
      mRNA expression in RPMC which was maximal after 12 hours in the absence of 
      cytokines, but which peaked after 2 hours when RPMC were challenged with asbestos 
      + TNF-alpha or IL-1 beta. Both types of asbestos also significantly increased 
      MCP-1 protein secretion after 24 and 48 hours (P < .0001), an effect that was 
      potentiated by cytokine stimulation. Rats exposed by inhalation to either 
      chrysotile or crocidolite asbestos fibers also had greater amounts of MCP-1 
      protein in their pleural lavage fluid than did sham-exposed rats. These findings 
      suggest that MCP-1 secretion by RPMC may have a role in the initiation and/or 
      potentiation of asbestos-induced pleural injury.
FAU - Tanaka, S
AU  - Tanaka S
AD  - Department of Pathology, Uniformed Services University of the Health Sciences, 
      Bethesda, Maryland 20814-4799, USA.
FAU - Choe, N
AU  - Choe N
FAU - Iwagaki, A
AU  - Iwagaki A
FAU - Hemenway, D R
AU  - Hemenway DR
FAU - Kagan, E
AU  - Kagan E
LA  - eng
GR  - HL-54196/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Exp Lung Res
JT  - Experimental lung research
JID - 8004944
RN  - 0 (Asbestos, Serpentine)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Mineral Fibers)
RN  - 0 (RNA, Messenger)
RN  - 12001-28-4 (Asbestos, Crocidolite)
RN  - 1332-21-4 (Asbestos)
SB  - IM
MH  - Animals
MH  - Asbestos/*pharmacology
MH  - Asbestos, Crocidolite/pharmacology
MH  - Asbestos, Serpentine/pharmacology
MH  - Cell Culture Techniques
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Cytokines/pharmacology
MH  - Epithelial Cells/*metabolism
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Inhalation Exposure
MH  - Male
MH  - Mineral Fibers
MH  - Pleura/chemistry/*cytology
MH  - RNA, Messenger/drug effects/metabolism
MH  - Rats
MH  - Rats, Inbred F344
EDAT- 2000/08/03 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/08/03 11:00
PHST- 2000/08/03 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/08/03 11:00 [entrez]
AID - 10.1080/019021400404528 [doi]
PST - ppublish
SO  - Exp Lung Res. 2000 Jun;26(4):241-55. doi: 10.1080/019021400404528.