Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
|
pubmed:dateCreated |
1996-9-26
|
pubmed:abstractText |
Monocytes are susceptible to HIV infection and to activation by a regulatory gene product of the HIV genome, HIV-Tat. Recently, we have demonstrated that treatment with HIV-Tat up-regulates monocyte adhesion to the endothelium and increases metalloproteinase production. in the present study, we have examined the ability of the HIV-Tat protein to alter the migratory and invasive behavior of monocytes. Monocytes pretreated for 24 h with 10 ng/ml HIV-Tat exhibited enhanced migratory behavior compared with untreated monocytes in chemotaxis assays, both in the absence of a chemoattractant as well as in response to FMLP. in addition, HIV-Tat itself induced the migration of both untreated and HIV-Tat pretreated monocytes. Checkerboard analysis showed that monocytes migrated in response to an HIV-Tat concentration gradient, thus confirming the chemotactic characteristics of the HIV-Tat protein. Pretreatment of monocytes with 10 ng/ml HIV-Tat for 24 h also increased their ability to invade reconstituted extracellular membrane (Matrigel)-coated filters by 5-fold in the absence of chemoattractant. The presence of FMLP or HIV-Tat further enhanced invasion by both untreated and HIV-Tat-pretreated monocytes by more than 10-fold. Monocyte invasion was partially inhibited by the inclusion of anti-beta integrin Ab or tissue inhibitor of metalloproteinase (TIMP). Thus, for the first time, we present evidence that HIV-Tat can enhance the chemotactic and invasive behaviors of monocytes and propose an active role for HIV-Tat in the recruitment of monocytes into extravascular tissues, a process which may contribute to the destruction of tissues and cellular architecture often seen in patients with acquired immunodeficiency syndrome.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
0022-1767
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
1
|
pubmed:volume |
157
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
974-7
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:8757599-Chemotaxis, Leukocyte,
pubmed-meshheading:8757599-Gene Products, tat,
pubmed-meshheading:8757599-HIV-1,
pubmed-meshheading:8757599-Humans,
pubmed-meshheading:8757599-Monocytes,
pubmed-meshheading:8757599-N-Formylmethionine Leucyl-Phenylalanine,
pubmed-meshheading:8757599-Time Factors,
pubmed-meshheading:8757599-tat Gene Products, Human Immunodeficiency Virus
|
pubmed:year |
1996
|
pubmed:articleTitle |
HIV-1-Tat protein promotes chemotaxis and invasive behavior by monocytes.
|
pubmed:affiliation |
Laboratories of Developmental Biology and Immunology, National Institute of Dental Research, National Institutes of Health, Bethesda, MD, USA.
|
pubmed:publicationType |
Journal Article
|