Expression of cell adhesion molecules at the surface of in vitro human immunodeficiency virus type 1-infected human monocytes: relationships with tumor necrosis factor alpha, interleukin 1beta, and interleukin 6 syntheses.
Further evidence suggests that cell adhesion molecules (CAMs) expressed on the surface of human immunodeficiency virus type 1 (HIV-1)-infected cells are regulated during lentiviral infection. To address this hypothesis we have investigated the kinetic pattern of CAM expression at the surface of HIV-1Ba.L-infected human monocytes during the first 72 hr of infection. A significantly lower expression of CD18 and CD54 as well as a decrease in CD44 expression level were observed at the surface of infected monocytes when compared with mock-infected cultures. No modification of CD11a, CD11b, CD11c, CD58, and CD62L expression was detected. Except for CD18, the expression of which at the cell surface is decreased, no modification of CD44 and CD54 expression was observed after heat-inactivated HIV-1 treatment of monocytes. Investigation of soluble forms of CAMs (sCAMs) and cytokine production in the culture supernatants of infected monocytes showed a peak of sCD44, TNF-alpha, IL-1beta, and IL-6 release between 2 and 24 hr after infection. Treatment of monocytes with monoclonal antibodies (MAbs) against CAMs showed that engagement of some CAMs may trigger TNF-alpha and IL-1beta production. In addition, pretreatment of infected monocytes with a TNF-alpha synthesis inhibitor, RP 55778, or with MAbs directed against IL-1beta, confirmed the role of TNF-alpha and IL-1beta in the regulation of CD18, CD44, and CD54 expression.
Le Naour
R
R
DSV/DRM, CRSSA, Institut Paris-Sud sur les Cytokines, Commissariat à l'Energie Atomique, Fontenay aux Roses, France.
Lussiez
C
C
Raoul
H
H
Mabondzo
A
A
Dormont
D
D
D000911:Antibodies, Monoclonal / Q000494:pharmacology; D018845:CD11 Antigens / Q000378:metabolism; D018821:CD18 Antigens / Q000378:metabolism; D018968:CD58 Antigens / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000276:immunology / Q000378:metabolism*; D016207:Cytokines / Q000096:biosynthesis*; D015658:HIV Infections / Q000276:immunology* / Q000378:metabolism*; D015497:HIV-1; D006801:Humans; D018960:Hyaluronan Receptors / Q000378:metabolism; D066298:In Vitro Techniques; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007375:Interleukin-1 / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D007700:Kinetics; D019041:L-Selectin / Q000378:metabolism; D009000:Monocytes / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D000093242:Interleukin-6 Inhibitors
D000911:Antibodies, Monoclonal; D018845:CD11 Antigens; D018821:CD18 Antigens; D018968:CD58 Antigens; D015815:Cell Adhesion Molecules; D016207:Cytokines; D018960:Hyaluronan Receptors; D018799:Intercellular Adhesion Molecule-1; D007375:Interleukin-1; D015850:Interleukin-6; D019041:L-Selectin; D014409:Tumor Necrosis Factor-alpha; D000093242:Interleukin-6 Inhibitors