PMID- 11145723
OWN - NLM
STAT- MEDLINE
DCOM- 20010308
LR  - 20190515
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 166
IP  - 2
DP  - 2001 Jan 15
TI  - HIV-1 Tat protein stimulates in vivo vascular permeability and lymphomononuclear 
      cell recruitment.
PG  - 1380-8
AB  - HIV-1 Tat protein released by infected cells is a chemotactic molecule for 
      leukocytes and induces a proinflammatory program in endothelial cells (EC) by 
      activating vascular endothelial growth factor (VEGF) receptors expressed on both 
      cell types. Its potential role in causing vascular permeability and leukocyte 
      recruitment was studied in vivo following its s.c. injection in mice. Tat caused 
      a dose-dependent early (15 min) and late (6 h) wave of permeability that were 
      inhibited by a neutralizing Ab anti-VEGF receptor type 2. Tissue infiltration of 
      lymphomononuclear cells, mainly monocytes (76%), was evident at 6 h and persisted 
      up to 24 h. WEB2170, a platelet activating factor (PAF) receptor antagonist, 
      reduced the early leakage by 70-80%, but only slightly inhibited the late wave 
      and cell recruitment. In vitro, Tat induced a dose-dependent flux of albumin 
      through the EC monolayer that was inhibited by Ab anti-vascular VEGF receptor 
      type 2 and WEB2170, and PAF synthesis in EC that was blocked by the Ab anti-VEGF 
      receptor type 2. Lastly, an anti-monocyte chemotactic peptide-1 (MCP-1) Ab 
      significantly reduced the lymphomononuclear infiltration elicited by Tat. In 
      vitro, Tat induced a dose-dependent production of MCP-1 by EC after a 24-h 
      stimulation. These results highlighted the role of PAF and MCP-1 as secondary 
      mediators in the onset of lymphomononuclear cell recruitment in tissues triggered 
      by Tat.
FAU - Arese, M
AU  - Arese M
AD  - Institute for Cancer Research and Treatment and Department of Genetics, Biology 
      and Biochemistry, School of Medicine, University of Torino, Candiolo. Italy.
FAU - Ferrandi, C
AU  - Ferrandi C
FAU - Primo, L
AU  - Primo L
FAU - Camussi, G
AU  - Camussi G
FAU - Bussolino, F
AU  - Bussolino F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Chemokines)
RN  - 0 (Gene Products, tat)
RN  - 0 (Platelet Activating Factor)
RN  - 0 (tat Gene Products, Human Immunodeficiency Virus)
SB  - IM
MH  - Animals
MH  - Capillary Permeability/*immunology
MH  - Cell Movement/*immunology
MH  - Cells, Cultured
MH  - Chemokines/physiology
MH  - Endothelium, Vascular/*immunology/pathology/virology
MH  - Gene Products, tat/*administration & dosage
MH  - HIV-1/*immunology
MH  - Humans
MH  - Injections, Subcutaneous
MH  - Lymphocytes/*immunology/pathology/virology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Monocytes/*immunology/pathology/virology
MH  - Platelet Activating Factor/biosynthesis/physiology
MH  - Skin/blood supply/metabolism/pathology/virology
MH  - Tumor Cells, Cultured
MH  - tat Gene Products, Human Immunodeficiency Virus
EDAT- 2001/01/06 11:00
MHDA- 2001/03/10 10:01
CRDT- 2001/01/06 11:00
PHST- 2001/01/06 11:00 [pubmed]
PHST- 2001/03/10 10:01 [medline]
PHST- 2001/01/06 11:00 [entrez]
AID - 10.4049/jimmunol.166.2.1380 [doi]
PST - ppublish
SO  - J Immunol. 2001 Jan 15;166(2):1380-8. doi: 10.4049/jimmunol.166.2.1380.