title: Elevated numbers of CD163+ macrophages in hearts of simian immunodeficiency virus-infected monkeys correlate with cardiac pathology and fibrosis.
abstract: The role of macrophage activation, traffic, and accumulation on cardiac pathology was examined in 23 animals. Seventeen animals were simian immunodeficiency virus (SIV) infected, 12 were CD8 lymphocyte depleted, and the remaining six were uninfected controls (two CD8 lymphocyte depleted, four nondepleted). None of the uninfected controls had cardiac pathology. One of five (20%) SIV-infected, non-CD8 lymphocyte-depleted animals had minor cardiac pathology with increased numbers of macrophages in ventricular tissue compared to controls. Seven of the 12 (58%) SIV-infected, CD8 lymphocyte-depleted animals had cardiac pathology in ventricular tissues, including macrophage infiltration and myocardial degeneration. The extent of fibrosis (measured as the percentage of collagen per tissue area) was increased 41% in SIV-infected, CD8 lymphocyte-depleted animals with cardiac pathology compared to animals without pathological abnormalities. The number of CD163+ macrophages increased significantly in SIV-infected, CD8 lymphocyte-depleted animals with cardiac pathology compared to ones without pathology (1.66-fold) and controls (5.42-fold). The percent of collagen (percentage of collagen per total tissue area) positively correlated with macrophage numbers in ventricular tissue in SIV-infected animals. There was an increase of BrdU+ monocytes in the heart during late SIV infection, regardless of pathology. These data implicate monocyte/macrophage activation and accumulation in the development of cardiac pathology with SIV infection.
authors: 1 Department of Biology, Boston College , Chestnut Hill, Massachusetts.
authors: Joshua A
authors: JA
authors: Walker
authors: Megan L
authors: ML
authors: Sulciner
authors: Katherine D
authors: KD
authors: Nowicki
authors: Andrew D
authors: AD
authors: Miller
authors: Tricia H
authors: TH
authors: Burdo
authors: Kenneth C
authors: KC
authors: Williams
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000097:blood* / Q000276:immunology; D015214:Antigens, Differentiation, Myelomonocytic / Q000097:blood* / Q000276:immunology; D001973:Bromodeoxyuridine / Q000032:analysis; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D005355:Fibrosis; D006352:Heart Ventricles / Q000166:cytology / Q000276:immunology / Q000473:pathology; D008212:Lymphocyte Depletion; D008253:Macaca mulatta; D008262:Macrophage Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D009000:Monocytes / Q000276:immunology / Q000473:pathology; D009205:Myocarditis / Q000473:pathology* / Q000821:virology; D009206:Myocardium / Q000276:immunology / Q000473:pathology*; D012367:RNA, Viral / Q000032:analysis; D011956:Receptors, Cell Surface / Q000097:blood* / Q000276:immunology; D012189:Retrospective Studies; D016097:Simian Acquired Immunodeficiency Syndrome / Q000150:complications / Q000276:immunology* / Q000473:pathology; D015302:Simian Immunodeficiency Virus / Q000276:immunology*; D014760:Viral Fusion Proteins / Q000032:analysis; D019562:Viral Load; D000098902:CD163 Antigen; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D001973:Bromodeoxyuridine; D012367:RNA, Viral; D011956:Receptors, Cell Surface; D014760:Viral Fusion Proteins; D000098902:CD163 Antigen; C067980:CD68 antigen, human; D000097382:CD68 Molecule