title: Ovine chlamydial abortion: characterization of the inflammatory immune response in placental tissues.
abstract: Ovine chlamydial abortion is a serious cause of fetal mortality in several sheep-rearing countries. The causal agent, Chlamydophila abortus (Chlamydia psittaci), does not generally induce clinical signs in the ewe other than abortion; this is associated with macroscopically visible damage in the placenta, which may be inflamed and thickened. To investigate the nature of the placental inflammation, seven pregnant sheep were inoculated subcutaneously at 70 days' gestation with C. abortus (strain S 26/3). A further five pregnant sheep received control inoculum by the same route at the same stage of pregnancy. Three of the infected ewes produced stillborn lambs and four produced live lambs. Lesions characteristic of chlamydial infection were present in all placentas except for two from one ewe that gave birth to twins. Histopathological examination of placental tissues from aborted fetuses showed a mixed inflammatory cell infiltrate with vasculitis and thrombosis in the mesenchyme of the intercotyledonary membranes. Cells expressing the macrophage-associated molecule CD 14 were found to be numerous, as were cells expressing major histocompatibility complex class II (MHC II) molecules. Many cells expressing messenger RNA (mRNA) encoding for tumour necrosis factor-alpha (TNF-alpha) were demonstrated, but few cells expressing interferon gamma mRNA and none expressing interleukin-4 mRNA were detected. The fetal immune response included small numbers of CD4+ and CD8+ cells, gamma delta T cells and B cells. It is concluded that abortion is the result of several factors, including destruction of tissue by C. abortus, vascular thrombosis, and an inflammatory response by the fetus. Production of TNF-alpha by fetal macrophages expressing MHC II molecules may be of considerable significance in the pathogenesis of abortion.
mesh_terms: D000034:Abortion, Veterinary / Q000209:etiology / Q000276:immunology / Q000473:pathology*; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D002691:Chlamydophila psittaci / Q000472:pathogenicity* / Q000502:physiology; D004195:Disease Models, Animal; D005260:Female; D005313:Fetal Death / Q000209:etiology / Q000276:immunology / Q000473:pathology / Q000662:veterinary; D005865:Gestational Age; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D016130:Immunophenotyping / Q000662:veterinary; D017403:In Situ Hybridization / Q000662:veterinary; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D010920:Placenta / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D011247:Pregnancy; D012333:RNA, Messenger / Q000378:metabolism; D012756:Sheep; D012757:Sheep Diseases / Q000276:immunology / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D000949:Histocompatibility Antigens Class II; D018950:Lipopolysaccharide Receptors; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma