title: Increased cardiac injury in NZB/W F1 mice received antibody against human parvovirus B19 VP1 unique region protein.
abstract: Human parvovirus B19 (B19) infection has been postulated to both myocardial injury and development of systemic lupus erythematosus (SLE). However, the influence of anti-B19-VP1u antibodies on cardiac disorders in SLE is still obscure. To elucidate the effects of anti-B19-VP1u IgG in SLE, passive transfer of PBS, normal rabbit IgG or rabbit anti-B19-VP1u IgG was injected intravenously into NZB/W F1 mice, respectively. Significant expression of IL-1β, IL-6 and TNF-α were detected in NZB/W F1 mice receiving rabbit anti-B19-VP1u IgG. Markedly cardiomyocyte disarray and lymphocyte infiltration were observed in left ventricle of hearts from NZB/W F1 mice receiving rabbit anti-B19-VP1u IgG. Additionally, significant increases of matrix metalloproteinase-9 (MMP9) activity and protein expression were detected in left ventricle of hearts from NZB/W F1 mice receiving B19-VP1u IgG. Accordingly, significant increase of phosphorylated p-38 and NF-κB proteins were observed in left ventricle of hearts from NZB/W F1 mice receiving B19-VP1u IgG. However, no significant variation of cardiac atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), heart-type fatty acid-binding protein (h-FABP) and creatine kinase MB (CK-MB) were detected among all experimental groups. These findings firstly demonstrated the aggravated effects of anti-B19 VP1u IgG on cardiac injury by induction of inflammatory but not myocardial infarction-associated proteins through activation of phosphorylated p-38 and NF-κB signaling.
authors.affiliation: Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung, Taiwan, ROC.
authors.forename: Bor-Show
authors.initials: BS
authors.lastname: Tzang
authors.forename: Tsung-Ming
authors.initials: TM
authors.lastname: Lin
authors.forename: Chun-Chou
authors.initials: CC
authors.lastname: Tsai
authors.forename: Jeng-Dong
authors.initials: JD
authors.lastname: Hsu
authors.forename: Lien-Chuan
authors.initials: LC
authors.lastname: Yang
authors.forename: Tsai-Ching
authors.initials: TC
authors.lastname: Hsu
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage* / Q000276:immunology; D036022:Capsid Proteins / Q000276:immunology*; D005260:Female; D006321:Heart; D006331:Heart Diseases / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D006352:Heart Ventricles / Q000473:pathology; D007116:Immunization, Passive; D015151:Immunoblotting; D007249:Inflammation; D053583:Interleukin-1beta / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000473:pathology; D008233:Lymphotoxin-alpha / Q000096:biosynthesis; D020780:Matrix Metalloproteinase 9 / Q000096:biosynthesis / Q000378:metabolism; D051379:Mice; D008814:Mice, Inbred NZB; D009203:Myocardial Infarction / Q000276:immunology / Q000473:pathology; D032383:Myocytes, Cardiac / Q000473:pathology*; D016328:NF-kappa B / Q000378:metabolism; D016732:Parvovirus B19, Human / Q000276:immunology*; D010766:Phosphorylation; D015398:Signal Transduction; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D036022:Capsid Proteins; D053583:Interleukin-1beta; D015850:Interleukin-6; D008233:Lymphotoxin-alpha; D016328:NF-kappa B; C095547:capsid protein VP1, parvovirus B19; D048051:p38 Mitogen-Activated Protein Kinases; D020780:Matrix Metalloproteinase 9