PMID- 10615068
OWN - NLM
STAT- MEDLINE
DCOM- 20000214
LR  - 20181130
IS  - 1044-1549 (Print)
IS  - 1044-1549 (Linking)
VI  - 22
IP  - 1
DP  - 2000 Jan
TI  - Bradykinin stimulates lung fibroblasts to release neutrophil and monocyte 
      chemotactic activity.
PG  - 75-84
AB  - Activation of the kallikrein-kinin system in lung injury has long been 
      recognized. However, the effects of bradykinin (BK) on human lung fibroblasts 
      (HLF) remain to be elucidated. We determined whether BK stimulates HLF to release 
      chemotactic activity for neutrophils and monocytes (NCA and MCA, respectively). 
      We evaluated HLF supernatant fluids for chemotactic activity through a blind-well 
      chamber technique. HLF released NCA and MCA in a dose- and time-dependent manner 
      in response to BK. The release of chemotactic activity was inhibited by 
      lipoxygenase inhibitors and cycloheximide. Molecular sieve column chromatography 
      revealed that both NCA and MCA had multiple chemotactic peaks. NCA was inhibited 
      by a leukotriene (LT) B(4) receptor antagonist and by antibodies to interleukin 
      (IL)-8 and granulocyte colony-stimulating factor (G-CSF). MCA was attenuated by 
      the LTB(4) receptor antagonist and by antibodies to monocyte chemoattractant 
      protein-1 (MCP-1), granulocyte-macrophage colony-stimulating factor (GM-CSF), and 
      transforming growth factor (TGF)-beta. Both the LTB(4) receptor antagonist and 
      these antibodies inhibited chemotactic activity of the molecular weights 
      corresponding to MCP-1, GM-CSF, and TGF-beta, separated by column chromatography. 
      The concentrations of IL-8, G-CSF, MCP-1, GM-CSF, and TGF-beta in supernatant 
      fluids increased significantly in a time-dependent manner in response to BK. The 
      receptors responsible for the release of NCA, MCA, and individual chemokines 
      included both BKB(1) and BKB(2) receptors. These data suggest that BK may 
      stimulate lung fibroblasts to release inflammatory cytokines, which may modulate 
      lung inflammation.
FAU - Koyama, S
AU  - Koyama S
AD  - First Department of Internal Medicine, Shinshu University School of Medicine, and 
      National Chushin-Matsumoto Hospital, Matsumoto, Japan.
FAU - Sato, E
AU  - Sato E
FAU - Numanami, H
AU  - Numanami H
FAU - Kubo, K
AU  - Kubo K
FAU - Nagai, S
AU  - Nagai S
FAU - Izumi, T
AU  - Izumi T
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipoxygenase Inhibitors)
RN  - 0 (Protein Synthesis Inhibitors)
RN  - 0 (Transforming Growth Factor beta)
RN  - 143011-72-7 (Granulocyte Colony-Stimulating Factor)
RN  - 1HGW4DR56D (Leukotriene B4)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - S8TIM42R2W (Bradykinin)
SB  - IM
MH  - Binding, Competitive
MH  - Bradykinin/metabolism/*physiology
MH  - Cells, Cultured
MH  - Chemokine CCL5/antagonists & inhibitors/metabolism
MH  - Chemotactic Factors/antagonists & inhibitors/isolation & purification/*metabolism
MH  - Chromatography, Gel
MH  - Fibroblasts/drug effects/*metabolism
MH  - Granulocyte Colony-Stimulating Factor/antagonists & inhibitors/metabolism
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/antagonists & 
      inhibitors/metabolism
MH  - Humans
MH  - Interleukin-8/antagonists & inhibitors/isolation & purification/*metabolism
MH  - Leukotriene B4/metabolism
MH  - Lipoxygenase Inhibitors/pharmacology
MH  - Lung/cytology/*metabolism
MH  - Macrophages, Alveolar
MH  - Monocytes/*metabolism
MH  - Protein Synthesis Inhibitors/pharmacology
MH  - Transforming Growth Factor beta/antagonists & inhibitors/metabolism
EDAT- 1999/12/30 09:00
MHDA- 2000/02/19 09:00
CRDT- 1999/12/30 09:00
PHST- 1999/12/30 09:00 [pubmed]
PHST- 2000/02/19 09:00 [medline]
PHST- 1999/12/30 09:00 [entrez]
AID - 10.1165/ajrcmb.22.1.3752 [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 2000 Jan;22(1):75-84. doi: 10.1165/ajrcmb.22.1.3752.