PMID- 7542307
OWN - NLM
STAT- MEDLINE
DCOM- 19950822
LR  - 20190516
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 58
IP  - 1
DP  - 1995 Jul
TI  - IL-1 activation of endothelium supports VLA-4 (CD49d/CD29)-mediated monocyte 
      transendothelial migration to C5a, MIP-1 alpha, RANTES, and PAF but inhibits 
      migration to MCP-1: a regulatory role for endothelium-derived MCP-1.
PG  - 71-9
AB  - We investigated the effect of interleukin-1 (IL-1) activation of human umbilical 
      vein endothelium (HUVE) on human monocyte transendothelial migration induced by 
      chemotactic factors. Monocyte migration across unactivated endothelium in 
      response to macrophage inflammatory protein-1 alpha (MIP-1 alpha), RANTES, 
      platelet-activating factor (PAF), or monocyte chemoattractant protein-1 (MCP-1) 
      was completely inhibited (90%) by monoclonal antibodies (mAbs; 60.3) to CD18 of 
      the CD11/CD18 complex on the monocyte and partially inhibited (by 75%) in 
      response to C5a. When the HUVE was stimulated with IL-1 alpha (5 h, 0.1 ng/ml), 
      monocyte migration in response to C5a, MIP-1 alpha, RANTES, or PAF was no longer 
      inhibited by mAb to CD18. However, migration was blocked by the combination of 
      mAb to the alpha 4-integrin (CD49d) chain of very late antigen-4 (CD49d/CD29) 
      with the mAb to CD18. In contrast to the above stimuli, activation of the HUVE 
      with IL-1 alpha inhibited the transendothelial migration of monocytes in response 
      to MCP-1. mAbs to the adhesion molecules up-regulated on HUVE by IL-1, i.e., 
      E-selectin (CD62E), intercellular adhesion molecule-1 (CD54) or vascular cell 
      adhesion molecule-1 (CD106), did not reverse the inhibitory effect. 
      Transendothelial migration in response to MCP-1 but not to C5a was inhibited by 
      the treatment of monocytes with culture supernatant from IL-1 alpha-stimulated 
      (but not from unstimulated) HUVE. Such supernatant contained chemotactic activity 
      for monocytes, and a mAb to MCP-1 blocked the migration inhibitory effect of IL-1 
      activation of the HUVE monolayer, as well as the chemotactic activity in the 
      supernatant from IL-1-stimulated HUVE. The inhibitory effect on migration of 
      IL-1-stimulated HUVE was specific for monocytes because polymorphonuclear 
      leukocyte transendothelial migration in response to IL-8 (a related chemokine) 
      was not inhibited by IL-1 activation of HUVE.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Chuluyan, H E
AU  - Chuluyan HE
AD  - Department of Pediatrics, Microbiology and Immunology, Dalhousie University, 
      Halifax, Nova Scotia, Canada.
FAU - Schall, T J
AU  - Schall TJ
FAU - Yoshimura, T
AU  - Yoshimura T
FAU - Issekutz, A C
AU  - Issekutz AC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Cytokines)
RN  - 0 (E-Selectin)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-8)
RN  - 0 (Lymphokines)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Monokines)
RN  - 0 (Platelet Activating Factor)
RN  - 0 (Protozoan Proteins)
RN  - 0 (Receptors, Very Late Antigen)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 80295-54-1 (Complement C5a)
SB  - IM
MH  - Cell Adhesion Molecules/physiology
MH  - Cells, Cultured
MH  - Chemokine CCL4
MH  - Chemokine CCL5
MH  - *Chemotaxis, Leukocyte
MH  - Complement C5a/*pharmacology
MH  - Cytokines/*pharmacology
MH  - E-Selectin
MH  - Endothelium, Vascular/*cytology/drug effects
MH  - In Vitro Techniques
MH  - Intercellular Adhesion Molecule-1/physiology
MH  - Interleukin-1/*pharmacology
MH  - Interleukin-8/pharmacology
MH  - Lymphokines/*pharmacology
MH  - Macrophage Inflammatory Proteins
MH  - Monocytes/*cytology
MH  - Monokines/*pharmacology
MH  - Neutrophils/physiology
MH  - Platelet Activating Factor/*pharmacology
MH  - Protozoan Proteins/*physiology
MH  - Receptors, Very Late Antigen/*metabolism
MH  - Vascular Cell Adhesion Molecule-1
EDAT- 1995/07/01 00:00
MHDA- 1995/07/01 00:01
CRDT- 1995/07/01 00:00
PHST- 1995/07/01 00:00 [pubmed]
PHST- 1995/07/01 00:01 [medline]
PHST- 1995/07/01 00:00 [entrez]
AID - 10.1002/jlb.58.1.71 [doi]
PST - ppublish
SO  - J Leukoc Biol. 1995 Jul;58(1):71-9. doi: 10.1002/jlb.58.1.71.