INTERLEUKIN-13 AND INTERLEUKIN-4 PROTECT BRONCHOALVEOLAR MACROPHAGES FROM PRODUCTIVE INFECTION WITH HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1

In this study, we examined the impact of the predominantly Th2-type ly mphokines interleukin 13 (IL-13) and interleukin 4 (IL-4) on acute inf ection of human bronchoalveolar macrophages with a macrophage-tropic i so- late of human immunodeficiency virus type 1 (HIV-1). Addition of 0 .01-10 ng of IL-4 or IL-13 per milliliters significantly blocked HIV-1 replication in infected cells, judging from levels of reverse transcr iptase and p24 antigen in the supernatants of infected cells. Both IL- 4 and IL-13 were almost as efficient as interferon-gamma (IFN-gamma) i n preventing HIV-1 replication, when given in equivalent amounts. More over, neither IL-13 nor IL-4 interfered with the IFN-gamma-mediated en hancement of anti-HIV-1 activity in alveolar macrophages. Both IL-4 an d IL-13 interfered with enhanced replication of HIV-1 in macrophages p ulsed with the growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF). Interleukin 13 also prevented HIV-1 release from per ipheral blood mononuclear cells in a cocultivation experiment with fee der cells from a seronegative subject. These data suggest that Th2-der ived lymphokines have significant anti-HIV-1 activity in cells of the macrophage lineage, although they may enhance the susceptibility of HI V-1-infected subjects to some opportunistic pathogens.