PMID- 7811465
OWN - NLM
STAT- MEDLINE
DCOM- 19950209
LR  - 20181130
IS  - 1044-1549 (Print)
IS  - 1044-1549 (Linking)
VI  - 12
IP  - 1
DP  - 1995 Jan
TI  - Regulation of monocyte chemoattractant protein-1 gene expression and secretion in 
      rat pulmonary alveolar macrophages by lipopolysaccharide, tumor necrosis 
      factor-alpha, and interleukin-1 beta.
PG  - 104-9
AB  - Chemotactic cytokines coordinate the recruitment of leukocytes into the lung 
      during pulmonary inflammation. In a previous study, we determined that rat 
      pulmonary alveolar macrophages (PAMs) facilitate monocyte recruitment and 
      activation in the lung during acute inflammatory lung injury, in part, through 
      the inducible expression of monocyte chemoattractant protein-1 (MCP-1). MCP-1 is 
      an 11 to 15 kD basic peptide that specifically mediates monocyte chemotaxis and 
      activation. Inflammatory mediators that regulate the expression and secretion of 
      MCP-1 by rat PAMs have not been identified. We determined that stimulation of 
      resident rat PAMs with bacterial lipopolysaccharide (LPS), murine tumor necrosis 
      factor-alpha, or human interleukin-1 beta resulted in the inducible expression of 
      MCP-1 mRNA and the secretion of biologically active MCP-1. In contrast, phorbol 
      myristate acetate, a nonphysiologic leukocyte activator, was significantly less 
      effective in stimulating either enhanced MCP-1 mRNA expression or secretion of 
      MCP-1. These results indicate that the expression of MCP-1 mRNA and the secretion 
      of MCP-1 by rat PAMs are regulated by bacterial products (LPS) and inflammatory 
      cytokines. Further, these results suggest PAMs are regulated by bacterial 
      products (LPS) and inflammatory cytokines. Further, these results suggest that 
      resident PAMs, through elaboration of MCP-1, may play a pivotal role in 
      regulating recruitment and activation of monocytes in the lung during acute 
      inflammatory lung injury.
FAU - Brieland, J K
AU  - Brieland JK
AD  - Unit for Laboratory Animal Medicine, University of Michigan Medical School, Ann 
      Arbor 48109-0614.
FAU - Flory, C M
AU  - Flory CM
FAU - Jones, M L
AU  - Jones ML
FAU - Miller, G R
AU  - Miller GR
FAU - Remick, D G
AU  - Remick DG
FAU - Warren, J S
AU  - Warren JS
FAU - Fantone, J C
AU  - Fantone JC
LA  - eng
GR  - HL-49136/HL/NHLBI NIH HHS/United States
GR  - RR-00200/RR/NCRR NIH HHS/United States
GR  - RR-07008/RR/NCRR NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (Alkaloids)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - H88EPA0A3N (Staurosporine)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Alkaloids/pharmacology
MH  - Animals
MH  - Base Sequence
MH  - Chemokine CCL2
MH  - Chemotactic Factors/*genetics/metabolism
MH  - Chemotaxis, Leukocyte
MH  - Gene Expression Regulation/*drug effects
MH  - Interleukin-1/*pharmacology
MH  - Lipopolysaccharides/*pharmacology
MH  - Macrophage Activation
MH  - Macrophages, Alveolar/drug effects/*metabolism
MH  - Male
MH  - Molecular Sequence Data
MH  - Protein Kinase C/antagonists & inhibitors/physiology
MH  - RNA, Messenger/biosynthesis
MH  - Rats
MH  - Specific Pathogen-Free Organisms
MH  - Staurosporine
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
AID - 10.1165/ajrcmb.12.1.7811465 [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 1995 Jan;12(1):104-9. doi: 
      10.1165/ajrcmb.12.1.7811465.