PMID- 9700081
OWN - NLM
STAT- MEDLINE
DCOM- 19980916
LR  - 20190312
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 275
IP  - 2
DP  - 1998 Aug
TI  - Human lung fibroblasts release chemokinetic activity for monocytes 
      constitutively.
PG  - L223-30
LID - 10.1152/ajplung.1998.275.2.L223 [doi]
AB  - We determined whether human lung fibroblasts (HLFs) might release mediators that 
      are responsible for monocyte chemokinetic activity (MCA) constitutively. HLF 
      supernatant fluids showed MCA in a time-dependent manner (P < 0.001). 
      Checkerboard analysis of 24- and 72-h supernatant fluids showed that the activity 
      was chemokinetic. Partial characterization of 24- and 72-h supernatant fluids 
      revealed that the mediators released after 24 h were predominantly composed of 
      lipid-soluble activity, and MCA was blocked by lipoxygenase inhibitors. The 
      mediators released after 72 h were predominantly trypsin sensitive and blocked by 
      cycloheximide. Molecular-sieve column chromatography identified four peaks of 
      MCA. A polyclonal antibody to monocyte chemoattractant protein-1 (MCP-1) 
      inhibited MCA by 20% after 24 h and by 40% after 72 h. Granulocyte-macrophage 
      colony-stimulating factor (GM-CSF) and transforming growth factor-beta (TGF-beta) 
      antibodies attenuated MCA released after 72 h by 30 and 10%, respectively. These 
      antibodies inhibited corresponding molecular-weight peaks separated by 
      molecular-sieve column. The concentrations of MCP-1, GM-CSF, and TGF-beta were 
      4,698 +/- 242, 26.8 +/- 3.8, and 550 +/- 15 pg/ml, respectively. A leukotriene B4 
      (LTB4)-receptor antagonist attenuated the total MCA and the lowest molecular 
      weight peak of MCA. The concentrations of LTB4 were 153.4 +/- 12.4 (24 h) and 212 
      +/- 16.6 (72 h) pg/ml. These findings suggest that HLFs may modulate the 
      recruitment of monocytes into the lung by releasing MCP-1, GM-CSF, TGF-beta, and 
      LTB4 constitutively.
FAU - Koyama, S
AU  - Koyama S
AD  - Shinshu University School of Medicine, First Department of Internal Medicine, 
      Matsumoto 390, Japan.
FAU - Sato, E
AU  - Sato E
FAU - Masubuchi, T
AU  - Masubuchi T
FAU - Takamizawa, A
AU  - Takamizawa A
FAU - Nomura, H
AU  - Nomura 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 Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Antibodies)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Lipoxygenase Inhibitors)
RN  - 0 (Platelet Activating Factor)
RN  - 0 (Receptors, Leukotriene B4)
RN  - 0 (Transforming Growth Factor beta)
RN  - 7BO8G1BYQU (Masoprocol)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - 98600C0908 (Cycloheximide)
RN  - EC 3.4.21.4 (Trypsin)
RN  - V867Q8X3ZD (Diethylcarbamazine)
SB  - IM
MH  - Adult
MH  - Antibodies
MH  - Cell Line
MH  - Chemokine CCL2/biosynthesis/metabolism
MH  - Chemokine CCL5/biosynthesis
MH  - *Chemotaxis, Leukocyte
MH  - Cycloheximide/pharmacology
MH  - Diethylcarbamazine/pharmacology
MH  - Fibroblasts/drug effects/metabolism/physiology
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/physiology
MH  - Humans
MH  - In Vitro Techniques
MH  - Kinetics
MH  - Lipoxygenase Inhibitors/pharmacology
MH  - Lung/*physiology
MH  - Masoprocol/pharmacology
MH  - Monocytes/*physiology
MH  - Platelet Activating Factor/antagonists & inhibitors
MH  - Receptors, Leukotriene B4/antagonists & inhibitors
MH  - T-Lymphocytes/immunology/physiology
MH  - Time Factors
MH  - Transforming Growth Factor beta/biosynthesis/physiology
MH  - Trypsin
EDAT- 1998/08/12 00:00
MHDA- 1998/08/12 00:01
CRDT- 1998/08/12 00:00
PHST- 1998/08/12 00:00 [pubmed]
PHST- 1998/08/12 00:01 [medline]
PHST- 1998/08/12 00:00 [entrez]
AID - 10.1152/ajplung.1998.275.2.L223 [doi]
PST - ppublish
SO  - Am J Physiol. 1998 Aug;275(2):L223-30. doi: 10.1152/ajplung.1998.275.2.L223.