PMID- 9469447
OWN - NLM
STAT- MEDLINE
DCOM- 19980226
LR  - 20171116
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 160
IP  - 4
DP  - 1998 Feb 15
TI  - Leishmania lipophosphoglycan reduces monocyte transendothelial migration: 
      modulation of cell adhesion molecules, intercellular junctional proteins, and 
      chemoattractants.
PG  - 1857-65
AB  - We previously identified the structural requirement for the inhibitory activity 
      of Leishmania lipophosphoglycan (LPG) to block endothelial adhesion to monocytes. 
      Here we showed that LPG reduces transendothelial migration of monocytes. LPG 
      pretreatment of endothelial cells (2 microM, 1 h) reduced monocyte migration 
      across endothelial cells activated by bacterial endotoxin (LPS) or IL-1beta (60 
      and 46%, respectively). A fragment of LPG (i.e., repeating phosphodisaccharide 
      (consisting of galactosyl-mannose)) and LPG coincubated with LPG-neutralizing mAb 
      lacks inhibitory activity on monocyte migration. Pretreatment of monocytes with 
      LPG (2 microM, 1 h) also did not affect monocyte migration through control or 
      LPS-activated endothelial cells. FACS analysis reveals that LPG treatment blocked 
      the LPS-mediated expression of E-selectin, intercellular adhesion molecule-1, and 
      vascular cell adhesion molecule-1 on endothelial cells and monocyte adhesion 
      without altering the integrity of the endothelial monolayer. LPG (2 microM, 1 h) 
      alone was capable of altering the expression and distribution of two junctional 
      adhesion molecules, CD31 and vascular endothelium cadherin, as well as reversing 
      the effects of LPS on these proteins. The induction of endothelial cells by LPS 
      to transcribe and release monocyte chemoattractant protein-1 (MCP-1) was 
      significantly reduced by LPG (40-65%). LPG treatment of nonactivated endothelial 
      cells also suppressed by 55 to 75% the monocyte migration triggered by a MCP-1 
      chemoattractant gradient, and coincubation of LPG with neutralizing mAb abrogated 
      the inhibitory activity. Together, these data point to a novel anti-inflammatory 
      function of LPG in reducing monocyte migration across endothelial cells via a 
      mechanism of inhibition of endothelial expression of cell adhesion molecules, 
      modulation of intercellular junctional proteins, and synthesis of MCP-1.
FAU - Lo, S K
AU  - Lo SK
AD  - Department of Medicine, Cornell University Medical College, NY 10021, USA. 
      sklo@mail.med.cornell.edu
FAU - Bovis, L
AU  - Bovis L
FAU - Matura, R
AU  - Matura R
FAU - Zhu, B
AU  - Zhu B
FAU - He, S
AU  - He S
FAU - Lum, H
AU  - Lum H
FAU - Turco, S J
AU  - Turco SJ
FAU - Ho, J L
AU  - Ho JL
LA  - eng
GR  - AI20941/AI/NIAID NIH HHS/United States
GR  - R29HL49883/HL/NHLBI NIH HHS/United States
GR  - R3722624/PHS 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  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Antigens, CD)
RN  - 0 (Cadherins)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Glycosphingolipids)
RN  - 0 (Platelet Endothelial Cell Adhesion Molecule-1)
RN  - 0 (cadherin 5)
RN  - 0 (lipophosphonoglycan)
SB  - IM
MH  - Animals
MH  - Antigens, CD
MH  - Cadherins/biosynthesis/metabolism
MH  - Cell Adhesion/drug effects/immunology
MH  - Cell Adhesion Molecules/biosynthesis/*metabolism
MH  - Cell Migration Inhibition
MH  - Chemokine CCL2/antagonists & inhibitors/biosynthesis/pharmacology
MH  - Chemotactic Factors/*metabolism
MH  - Chemotaxis, Leukocyte/drug effects/*immunology
MH  - Endothelium, Vascular/drug effects/*immunology
MH  - Glycosphingolipids/*pharmacology
MH  - Humans
MH  - Intercellular Junctions/immunology/*metabolism
MH  - Leishmania donovani/*immunology
MH  - Monocytes/*immunology/physiology
MH  - Platelet Endothelial Cell Adhesion Molecule-1/biosynthesis/metabolism
EDAT- 1998/02/20 00:00
MHDA- 1998/02/20 00:01
CRDT- 1998/02/20 00:00
PHST- 1998/02/20 00:00 [pubmed]
PHST- 1998/02/20 00:01 [medline]
PHST- 1998/02/20 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1998 Feb 15;160(4):1857-65.