title: Pulmonary intravascular monocytes/macrophages in a rat model of sepsis.
abstract: Sepsis induces recruitment of neutrophils and monocytes/macrophages in the lung and enhances host susceptibility to a secondary bacterial challenge. The phenotype and functions of recruited pulmonary intravascular monocytes/macrophages (PIMMs) in sepsis remain largely unknown. Therefore, we characterized PIMM recruitment and functions in a rat model of E. coli-induced sepsis. Male Sprague-Dawley rats were injected intraperitoneally with saline (n=10) and 48 hr after the saline treatment treated intravenously with either saline (n=5) or E. coli lipopolysachharide (LPS; 1.5 microg/kg body weight; n=5). A second group of 10 rats was infected intraperitoneally with E. coli (2x10(7) CFU/100 g) followed by intravenous injection of either saline (n=5) or LPS (n=5) 48 hr after the first treatment. Rats were euthanized at 6 hr after LPS treatment. Immunocytochemistry showed more PIMMs stained with ED-1 antibody, which specifically reacts with rat monocytes/macrophages, in rats infected with E. coli compared with the controls (P<0.05). LPS treatment of E. coli-infected rats increased the numbers of PIMMs (P<0.05) and induced more inflammation compared to other groups. Immuno-electron microscopy localized TNF-alpha, IL-10, and TGF-beta2 in recruited PIMMs in rats challenged with both E. coli and LPS. ELISA on lung homogenates showed higher concentrations of TNF-alpha, IL-10, and TGF-beta2 in rats treated with both E. coli and LPS compared with those treated with only LPS or E. coli (P<0.05). We conclude that ED-1-positive PIMMs are recruited in this model of sepsis and contain TNF-alpha, IL-10, and TGF-beta2.
authors.affiliation: Immunology Research Group and Department of Veterinary Biomedical Sciences, University of Saskatchewan, Saskatoon, Canada.
authors.forename: Chandrashekhar
authors.initials: C
authors.lastname: Charavaryamath
authors.forename: Kyathanahalli S
authors.initials: KS
authors.lastname: Janardhan
authors.forename: Sarah
authors.initials: S
authors.lastname: Caldwell
authors.forename: Baljit
authors.initials: B
authors.lastname: Singh
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D000941:Antigens / Q000032:analysis; D004195:Disease Models, Animal; D004927:Escherichia coli Infections / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D007150:Immunohistochemistry; D016753:Interleukin-10 / Q000032:analysis; D008070:Lipopolysaccharides / Q000378:metabolism; D008168:Lung / Q000737:chemistry / Q000276:immunology / Q000473:pathology* / Q000648:ultrastructure; D016676:Macrophages, Alveolar / Q000737:chemistry / Q000276:immunology / Q000648:ultrastructure*; D008297:Male; D016253:Microscopy, Immunoelectron; D009000:Monocytes / Q000737:chemistry / Q000276:immunology / Q000648:ultrastructure*; D018410:Pneumonia, Bacterial / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D053781:Transforming Growth Factor beta2 / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D000911:Antibodies, Monoclonal; D000941:Antigens; D008070:Lipopolysaccharides; C509043:Tgfb2 protein, rat; D053781:Transforming Growth Factor beta2; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10