       Document 0737
 DOCN  M9440737
 TI    Human immunodeficiency virus type 1 infection of human macrophages
       modulates the cytokine response to Pneumocystis carinii.
 DT    9404
 AU    Kandil O; Fishman JA; Koziel H; Pinkston P; Rose RM; Remold HG; Division
       of Pulmonary and Critical Medicine, New England; Deaconess Hospital,
       Boston, Massachusetts.
 SO    Infect Immun. 1994 Feb;62(2):644-50. Unique Identifier : AIDSLINE
       MED/94131601
 AB    The present studies examined production of the cytokines tumor necrosis
       factor alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IL-6 by
       human monocyte-derived macrophages exposed to Pneumocystis carinii in
       vitro and the impact of concurrent macrophage infection with human
       immunodeficiency virus type 1 (HIV-1) on these cytokine responses.
       Macrophages were infected with the HIV-1 BaL monocytotropic strain for
       10 to 14 days and then exposed to P. carinii. At various times following
       P. carinii treatment, culture supernatants were harvested to assess the
       cytokine profile. Addition of P. carinii to HIV-uninfected macrophages
       resulted in augmented production of IL-6, TNF-alpha, and IL-1 beta
       protein. By contrast, in HIV-infected macrophages exposed to P. carinii,
       only the release of IL-6 was increased compared with that for
       HIV-uninfected macrophages, while the levels of TNF-alpha and IL-1 beta
       decreased. This altered response was confirmed at the molecular level
       for TNF-alpha mRNA. Preventing physical contact between P. carinii and
       macrophages by a membrane filter inhibited all cytokine release.
       Substituting P. carinii with a preparation of P. carinii 95- to 115-kDa
       major membrane glycoprotein A yielded a response similar to that
       obtained by addition of intact P. carinii. These results suggest that
       HIV-1 infection of human macrophages modulates cytokine responses to P.
       carinii.
 DE    AIDS-Related Opportunistic Infections/ETIOLOGY  Cell Adhesion/IMMUNOLOGY
       Cytokines/*BIOSYNTHESIS  Fungal Proteins/IMMUNOLOGY  Human  HIV
       Infections/*MICROBIOLOGY  *HIV-1  In Vitro  Interleukin-1/BIOSYNTHESIS
       Interleukin-6/BIOSYNTHESIS  Macrophages/*IMMUNOLOGY/MICROBIOLOGY
       Membrane Glycoproteins/IMMUNOLOGY  Pneumocystis carinii/*IMMUNOLOGY
       Pneumonia, Pneumocystis carinii/ETIOLOGY  RNA,
       Messenger/GENETICS/METABOLISM  Support, Non-U.S. Gov't  Support, U.S.
       Gov't, P.H.S.  Tumor Necrosis Factor/BIOSYNTHESIS/GENETICS  JOURNAL
       ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

