fibrin and Swine-Diseases

Topics: Animals; Blood Coagulation; Brain; Cattle; Cattle Diseases; Disseminated Intravascular Coagulation; Dog Diseases; Dogs; Fibrin; Heparin; Lung; Myocardium; Swine; Swine Diseases

Obesity is associated with increased serum fibrinogen level. Myostatin (MSTN), a strong inhibitor of skeletal muscle growth, is recognized as a potential target for obesity. However, the effect of MSTN inhibition on fibrinogen is not largely known. The objective of the present study was to explore fibrinogen levels after MSTN inhibition. Fibrinogen levels and the fibrin clot structure of MSTN homozygous knockout (KO) and wild-type (WT) pigs (n = 4 in each group) were investigated. The protein expression of fibrinogen in the serum and liver of KO pigs decreased greatly (1.6-fold loss for serum and 2.5-fold loss for liver). KO pigs showed significantly decreased gene expression of fibrinogen chains: FGA (fibrinogen-α; 11-fold), FGB (fibrinogen-β; 8-fold) and FGG (fibrinogen-γ; 7.4-fold). The basal transcriptional regulators of fibrinogen, HNF1 (hepatocyte nuclear factor 1) and CEBP-α (CCAAT/Enhancing-binding protein-alpha) were remarkably down-regulated after interruption of MSTN expression by siRNA (small interfering RNA) in cultured hepatocytes (about 2- and 4-fold, respectively). Compared with WT pigs, KO pigs displayed altered fibrin clot structure with thinner fibers, decreased turbidity and increased permeability. The findings indicate that the inhibition of MSTN could affect fibrinogen levels and the fibrin clot structure.

Topics: Animals; Fibrin; Fibrinogen; Homozygote; Muscle, Skeletal; Myostatin; Obesity; Swine; Swine Diseases

Chronic pneumonia experimentally produced in 14 pigs with African swine fever (ASF) virus was studied by immunofluorescene (IF) and histopathologic techniques. Frozen sections prepared from pulmonary tissues of the infected pigs were stained with fluorescein-conjugated antiserums against ASF viral antigen, porcine immunoglobulin G (IgG), procine complement (C), and porcine fibrinogen. The viral antigen(s) was mainly seen in macrophages and cell debris in alveolar walls and lumens. This finding indicates that the virus replicated in the cytoplasm of alveolar macrophages that subsequently degenerated and released the viral antigen. Diffuse immunoglobulin (Ig) deposition was found in necrotic cells and debris. Immunoglobulin also was seen bound to intracytoplasmic inclusion bodies in some degenerating alveolar macrophages. This finding indicates that antibody against ASF viral antigen(s) excluded from blood circulation or produced by local immunocytes (or both) reacted with viral antigen at intramacrophage and extramacrophage levels and resulted in the formation of insoluble antigen-antibody (Ag-Ab) complexes. The participation of C in the immune complex was evident in the early stage of the pneumonia, but was less evident in the subsequent extensive, progressive necrotic processes. Fibrin deposits were visible only in the early necrotic area of alveolar walls and lumens. Possible mechanisms inducing extensive necrosis are discussed.

Topics: African Swine Fever; Animals; Antigen-Antibody Complex; Antigens, Viral; Complement System Proteins; DNA Viruses; Fibrin; Fibrinogen; Fluorescent Antibody Technique; Immune Sera; Immunoglobulin G; Lung; Macrophages; Necrosis; Pneumonia, Viral; Pulmonary Alveoli; Rabbits; Swine; Swine Diseases

Topics: Animals; Basement Membrane; Bronchi; Cell Differentiation; Collagen; Connective Tissue Cells; Elastic Tissue; Epithelium; Fibrin; Fibroblasts; Histocytochemistry; Lung; Macrophages; Microscopy, Electron; Mitosis; Muscle, Smooth; Necrosis; Pseudorabies; Swine; Swine Diseases

Topics: Animals; Arthritis; Carrageenan; Fibrin; Germ-Free Life; Hypertrophy; Lymphocytes; Phagocytosis; Rabbits; Swine; Swine Diseases; Synovial Fluid; Synovial Membrane