PMID- 9068082
OWN - NLM
STAT- MEDLINE
DCOM- 19970801
LR  - 20190914
IS  - 1073-2322 (Print)
IS  - 1073-2322 (Linking)
VI  - 7
IP  - 3
DP  - 1997 Mar
TI  - Reconstituted high density lipoprotein modulates adherence of polymorphonuclear 
      leukocytes to human endothelial cells.
PG  - 175-81
AB  - A reconstituted high density lipoprotein (rHDL) containing human apolipoprotein 
      A-I and phosphatidylcholine was tested for its ability to modify 
      polymorphonuclear leukocyte (PMN) adherence to endothelial cells (EC) in vitro. 
      EC stimulation for 4 h with lipopolysaccharide (LPS) or tumor necrosis 
      factor-alpha (TNF alpha) resulted in a four- to sixfold increase in PMN 
      adherence. Concomitant stimulation of EC with LPS and rHDL virtually prevented 
      the LPS-stimulated increase in PMN adherence. Changes in adherence were 
      paralleled by alterations in adhesion molecule expression of EC. Concomitant EC 
      stimulation with LPS and rHDL resulted in complete inhibition of the 
      LPS-stimulated increase in expression of E-selectin and intercellular adhesion 
      molecule 1 (ICAM-1). In contrast, rHDL reduced the TNF alpha-induced expression 
      of adhesion molecules as well as the PMN adherence to TNF alpha-stimulated EC by 
      approximately 10%. The CD11/CD18-mediated PMN adherence to EC as a consequence of 
      PMN stimulation with calcium ionophore (A23187) was diminished in the presence of 
      rHDL after 7 min incubation by 36.1 +/- 11.4% and after 15 min incubation by 45.1 
      +/- 7.4%. In addition, the A23187-stimulated increase in PMN adherence to 
      fibrinogen-coated surfaces, mediated by CD11b/CD18, was virtually eliminated in 
      the presence of rHDL and HDL, but not in the presence of apolipoprotein A-I or 
      natural low density lipoprotein. FACS analysis showed that PMN treated with rHDL 
      and subsequently washed were resistant to FMLP-induced CD11b/ CD18 up-regulation. 
      In conclusion, these data indicate that rHDL decreases cell adhesion via two 
      mechanisms: blocking LPS activity and modifying CD11b/CD18 up-regulation on PMN.
FAU - Moudry, R
AU  - Moudry R
AD  - ZLB Central Laboratory, Blood Transfusion Service, Swiss Red Cross, Bern, 
      Switzerland.
FAU - Spycher, M O
AU  - Spycher MO
FAU - Doran, J E
AU  - Doran JE
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Apolipoprotein A-I)
RN  - 0 (CD11 Antigens)
RN  - 0 (CD18 Antigens)
RN  - 0 (E-Selectin)
RN  - 0 (Integrins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Lipoproteins, HDL)
RN  - 0 (Macrophage-1 Antigen)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 37H9VM9WZL (Calcimycin)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
RN  - 9001-32-5 (Fibrinogen)
SB  - IM
MH  - Apolipoprotein A-I/pharmacology
MH  - CD11 Antigens/metabolism
MH  - CD18 Antigens/metabolism
MH  - Calcimycin/pharmacology
MH  - Cell Adhesion/physiology
MH  - Cells, Cultured
MH  - E-Selectin/metabolism
MH  - Endothelium, Vascular/*cytology
MH  - Fibrinogen/pharmacology
MH  - Humans
MH  - Integrins/metabolism
MH  - Intercellular Adhesion Molecule-1/biosynthesis
MH  - Lipopolysaccharides/pharmacology
MH  - Lipoproteins, HDL/*physiology
MH  - Macrophage-1 Antigen/metabolism
MH  - N-Formylmethionine Leucyl-Phenylalanine/pharmacology
MH  - Neutrophils/*cytology/immunology
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1997/03/01 00:00
MHDA- 1997/03/01 00:01
CRDT- 1997/03/01 00:00
PHST- 1997/03/01 00:00 [pubmed]
PHST- 1997/03/01 00:01 [medline]
PHST- 1997/03/01 00:00 [entrez]
AID - 10.1097/00024382-199703000-00004 [doi]
PST - ppublish
SO  - Shock. 1997 Mar;7(3):175-81. doi: 10.1097/00024382-199703000-00004.