title: Is decreased HIV-1 infectivity of placental macrophages caused by high levels of beta-chemokines?
abstract: The objective of this study was to determine the effect of beta-chemokine secretion on HIV infection of placental macrophages (HF) as compared to monocyte-derived macrophages (MDM). For this purpose, we measured chemokine production in supematants of LPS stimulated and unstimulated HF and MDM. LPS stimulated cultures produced 3 to 10 times higher levels of MIP-1alpha, MIP-1beta and RANTES than unstimulated cultures. The level of MIP-1beta was the highest of the three chemokines secreted upon stimulation of HF cells. Cell cultures were inoculated with HIV-BaL, a R5 virus, and tested for p24 antigen and chemokine production at days 5 and 10 post-infection (P.I.). We did not find significant differences in the level of chemokines produced by HIV-1-infected and uninfected MDM and HF cells. However, significant differences were found in p24 antigen released by unstimulated and LPS stimulated cells. In contrast to HF cells, MDM cultures showed a significant inhibition of p24 antigen production when cells were stimulated with LPS prior to infection. HF cells were less susceptible to HIV-1 infection than MDM, and chemokines produced by HF cells did not result in further inhibition of HIV-1 infection. We found that in contrast to MDM, decreased susceptibility HF cells to HIV infection is not due to increased levels of chemokines, but to decreased HIV-1 coreceptor expression.
authors.affiliation: The Univ. of Puerto Rico School of Medicine, Dept. of Microbiology and Medical Zoology, San Juan 00936-5067, USA.
authors.forename: J
authors.initials: J
authors.lastname: Meléndez
authors.forename: V
authors.initials: V
authors.lastname: García
authors.forename: E
authors.initials: E
authors.lastname: Sánchez
authors.forename: R
authors.initials: R
authors.lastname: Delgado
authors.forename: G
authors.initials: G
authors.lastname: Torres
authors.forename: L M
authors.initials: LM
authors.lastname: Meléndez-Guerrero
mesh_terms: D015704:CD4 Antigens / Q000378:metabolism; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000096:biosynthesis; D018925:Chemokines / Q000096:biosynthesis*; D005260:Female; D016655:HIV Core Protein p24 / Q000378:metabolism; D015658:HIV Infections / Q000150:complications / Q000276:immunology / Q000821:virology; D015497:HIV-1 / Q000187:drug effects / Q000276:immunology* / Q000472:pathogenicity* / Q000502:physiology; D006801:Humans; D066298:In Vitro Techniques; D008070:Lipopolysaccharides / Q000494:pharmacology; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis; D008264:Macrophages / Q000187:drug effects / Q000276:immunology* / Q000821:virology*; D010920:Placenta / Q000276:immunology* / Q000821:virology*; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000276:immunology / Q000821:virology; D019713:Receptors, CCR5 / Q000378:metabolism; D019718:Receptors, CXCR4 / Q000378:metabolism; D014779:Virus Replication / Q000187:drug effects
chemical_list: D015704:CD4 Antigens; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D018925:Chemokines; D016655:HIV Core Protein p24; D008070:Lipopolysaccharides; D019402:Macrophage Inflammatory Proteins; D019713:Receptors, CCR5; D019718:Receptors, CXCR4