Prevention of myosin-induced autoimmune myocarditis in mice by anti-L3T4 monoclonal antibody

2003 ◽  
Vol 81 (2) ◽  
pp. 84-88 ◽  
Author(s):  
Hai-Tao Yuan ◽  
Yu-Hua Liao ◽  
Zhaohui Wang ◽  
Ji-Hua Dong ◽  
Lin-Sheng Cao ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Immune Tolerance ◽  
Light Microscope ◽  
Myocardial Injury ◽  
Inflammatory Cells ◽  
Treated Group ◽  
Cardiac Myosin ◽  
Pathological Changes ◽  
Autoimmune Myocarditis ◽  
Myocardial Degeneration

This study was aimed at studying the effect of the induction of immune tolerance to swine cardiac myosin from anti-L3T4 monoclonal antibody injection and whether the immune tolerance could protect mice with myosin-induced myocarditis from myocardial injury. Twenty-four Balb/c mice were divided into two groups at random. All of the mice were immunized with swine cardiac myosin on the 1st day, 14th, 28th, 42nd, and 52nd day. Immune tolerance was induced by triplicate injections of 400 μg anti-L3T4 McAb on the 0 day (intravenous), 1st day, and 2nd day (intraperitoneal) in McAb-treated group. In the saline-treated group, saline of the same volume as anti-L3T4 monoclonal antibody was used as a control. The sera and hearts biopsies of all mice were collected on the 58th day. The anti-cardiac myosin antibody was examined with ELISA, and pathological changes of heart were observed by light microscope. It was shown that mice immunized with swine cardiac myosin could produce anti-myosin antibody and the anti-cardiac myosin antibody was positive in most of the saline-treated group but negative in the McAb-treated group. Morphologically, myocardial degeneration, necrosis, and infiltration of inflammatory cells were found in the saline-treated group but not in the McAb-treated group. In conclusion, this study indicated that the immune tolerance to cardiac myosin was induced by the anti-L3T4 monoclonal antibody, and accordingly myocardial injury could be prevented by induction of immune tolerance.Key words: anti-L3T4 monoclonal antibody, myosin, immune tolerance, myocarditis.

Immune Tolerance to Cardiac Myosin Induced by Anti-CD4 Monoclonal Antibody in Autoimmune Myocarditis Rats

2006 ◽  
Vol 26 (3) ◽  
pp. 213-221 ◽  
Author(s):  
Wang Qing-Qing ◽  
Wang Yu-Lin ◽  
Yuan Hai-Tao ◽  
Liu Feng-Qin ◽  
Jin You-Peng ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Immune Tolerance ◽  
Cardiac Myosin ◽  
Autoimmune Myocarditis

Cardioprotective effects of omega 3 fatty acids from fish oil and it enhances autoimmunity in porcine cardiac myosin-induced myocarditis in the rat model

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Ling-Yan Li ◽  
Xu Wang ◽  
Ting-Chuan Zhang ◽  
Zong-Jun Liu ◽  
Jun-Qing Gao
Keyword(s):  
Fatty Acids ◽  
Fish Oil ◽  
Inflammatory Cells ◽  
Omega 3 Fatty Acids ◽  
Cardiac Myosin ◽  
Omega 3 ◽  
Autoimmune Myocarditis ◽  
Tuna Fish ◽  
Fame Analysis ◽  
Total Fatty Acids

Abstract This experiment proposed to investigate the efficiency of omega 3 fatty acids from fish that improves autoimmune against myocarditis in the rat. Fish oil was extracted from fresh Tuna fish and performed FAME analysis and mice bioassay. The autoimmune myocarditis was induced by subcutaneous injection of porcine cardiac myosin (PCM) into the footpads of rats on the first and seventh day. Rats were dissected on the 21st day to analyze the histopathological, hemodynamic, echocardiographic factors, and immunohistochemistry expressions. In the study, 73.90% of total fatty acids were recorded. Histological analysis revealed that omega 3 fatty acids administrated groups showed tremendous development in the multifocal myocardia hyaline degeneration and necrosis with inflammatory changes. Moreover, omega 3 fatty acids inhabited the expressions of inflammatory cells (CD4, CD8 and CD11b) and suppressed the level of NF-κB. The echocardiographic factors such as heartbeat, SBP, DBP, levels of LVDs, LVDd, LVPW percentage of LVFS, EF, expression levels of inflammatory cytokines (TNF, IL-1β, IFN-ɤ, IL-2, and IL-6) also significantly suppressed by omega 3 fatty acids. Hence, the present study proved that consuming fatty acid-enriched fish might be a successful therapy for improving the inflammatory profile, regenerates the heart tissues, and controlled the production of inflammatory cells.

scholarly journals Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats

2012 ◽  
Vol 303 (9) ◽  
pp. H1114-H1127 ◽  
Author(s):  
Pablo Nakagawa ◽  
Yunhe Liu ◽  
Tang-Dong Liao ◽  
Xiaojuan Chen ◽  
Germán E. González ◽  
...  
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Adhesion Molecules ◽  
Cardiac Dysfunction ◽  
Myocardial Injury ◽  
Cardiac Myosin ◽  
Autoimmune Myocarditis ◽  
Cell Responses ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune

Myocarditis is commonly associated with cardiotropic infections and has been linked to development of autoimmunity. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring tetrapeptide that prevents inflammation and fibrosis in hypertension and other cardiovascular diseases; however, its effect on autoimmune-mediated cardiac diseases remains unknown. We studied the effects of Ac-SDKP in experimental autoimmune myocarditis (EAM), a model of T cell-mediated autoimmune disease. This study was conducted to test the hypothesis that Ac-SDKP prevents autoimmune myocardial injury by modulating the immune responses. Lewis rats were immunized with porcine cardiac myosin and treated with Ac-SDKP or vehicle. In EAM, Ac-SDKP prevented both systolic and diastolic cardiac dysfunction, remodeling as shown by hypertrophy and fibrosis, and cell-mediated immune responses without affecting myosin-specific autoantibodies or antigen-specific T cell responses. In addition, Ac-SDKP reduced cardiac infiltration by macrophages, dendritic cells, and T cells, pro-inflammatory cytokines [interleukin (IL)-1α, tumor necrosis factor-α, IL-2, IL-17] and chemokines (cytokine-induced neutrophil chemoattractant-1, interferon-γ-induced protein 10), cell adhesion molecules (intercellular adhesion molecule-1, L-selectin), and matrix metalloproteinases (MMP). Ac-SDKP prevents autoimmune cardiac dysfunction and remodeling without reducing the production of autoantibodies or T cell responses to cardiac myosin. The protective effects of Ac-SDKP in autoimmune myocardial injury are most likely mediated by inhibition of 1) innate and adaptive immune cell infiltration and 2) expression of proinflammatory mediators such as cytokines, chemokines, adhesion molecules, and MMPs.

Biological variation of cardiac myosin-binding protein C in healthy individuals

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Bashir Alaour ◽  
Torbjørn Omland ◽  
Janniche Torsvik ◽  
Thomas E. Kaier ◽  
Marit S. Sylte ◽  
...  
Keyword(s):  
Risk Stratification ◽  
Protein C ◽  
Myocardial Injury ◽  
Binding Protein ◽  
Biological Variation ◽  
Cardiac Myosin ◽  
Analytical Quality ◽  
Myosin Binding Protein ◽  
Myosin Binding Protein C ◽  
Myosin Binding

Abstract Objectives Cardiac myosin-binding protein C (cMyC) is a novel biomarker of myocardial injury, with a promising role in the triage and risk stratification of patients presenting with acute cardiac disease. In this study, we assess the weekly biological variation of cMyC, to examine its potential in monitoring chronic myocardial injury, and to suggest analytical quality specification for routine use of the test in clinical practice. Methods Thirty healthy volunteers were included. Non-fasting samples were obtained once a week for ten consecutive weeks. Samples were tested in duplicate on the Erenna® platform by EMD Millipore Corporation. Outlying measurements and subjects were identified and excluded systematically, and homogeneity of analytical and within-subject variances was achieved before calculating the biological variability (CVI and CVG), reference change values (RCV) and index of individuality (II). Results Mean age was 38 (range, 21–64) years, and 16 participants were women (53%). The biological variation, RCV and II with 95% confidence interval (CI) were: CVA (%) 19.5 (17.8–21.6), CVI (%) 17.8 (14.8–21.0), CVG (%) 66.9 (50.4–109.9), RCV (%) 106.7 (96.6–120.1)/−51.6 (−54.6 to −49.1) and II 0.42 (0.29–0.56). There was a trend for women to have lower CVG. The calculated RCVs were comparable between genders. Conclusions cMyC exhibits acceptable RCV and low II suggesting that it could be suitable for disease monitoring, risk stratification and prognostication if measured serially. Analytical quality specifications based on biological variation are similar to those for cardiac troponin and should be achievable at clinically relevant concentrations.

scholarly journals Depletion of alpha/beta T cells by a monoclonal antibody against the alpha/beta T cell receptor suppresses established adjuvant arthritis, but not established collagen-induced arthritis in rats.

1992 ◽  
Vol 175 (4) ◽  
pp. 907-915 ◽  
Author(s):  
S Yoshino ◽  
L G Cleland
Keyword(s):  
Monoclonal Antibody ◽  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Adjuvant Arthritis ◽  
Inflammatory Cells ◽  
Cell Receptor ◽  
Collagen Induced Arthritis ◽  
Alpha Beta ◽  
Synovial Tissues

The effects of treatment with a monoclonal antibody (R73 mAb) against T cell receptor alpha/beta (TCR-alpha/beta) on both established adjuvant arthritis (EAA) and established collagen-induced arthritis (ECIA) in rats have been investigated. Rats were treated with R73 mAb when arthritis reached a peak. Treatment with the anti-TCR-alpha/beta mAb markedly suppressed EAA, whereas ECIA was not affected by the mAb treatment. Histologically, R73 mAb-treated rats with EAA showed mild hyperplasia of synovial tissues, sparse infiltration of inflammatory cells, and minimal erosion of cartilage, whereas arthritic rats treated with PBS and an irrelevant control mAb against Giardia had marked hyperplasia of synovium with pannus, massive inflammatory cell infiltrate, and severe destruction of cartilage and subchondral bone. R73 mAb-treated rats with ECIA exhibited pronounced formation of pannus containing many inflammatory cells and marked cartilage and subchondral damage similar to those in arthritic rats that received the control treatments. Treatment with R73 mAb depleted markedly alpha/beta+ T cells in both peripheral blood and synovial tissues of rats with EAA and ECIA. R73 mAb treatment was associated with marked reduction in arthritogen-specific delayed-type hypersensitivity responses in both EAA and ECIA. The titers of antibodies against type II collagen produced in rats with ECIA were not affected by the mAb. Thus, alpha/beta+ T cells appear to have a central role in EAA, but not in chronic ECIA.

scholarly journals High Mortality with Severe Dystrophic Cardiac Calcinosis in C3H/OUJ Mice Fed High Fat Purified Diets

1988 ◽  
Vol 25 (2) ◽  
pp. 113-118 ◽  
Author(s):  
J. I. Everitt ◽  
L. M. Olson ◽  
J. B. Mangum ◽  
W. J. Visek
Keyword(s):  
High Fat Diet ◽  
Inflammatory Cell ◽  
Mouse Strains ◽  
Cardiovascular Collapse ◽  
Pathological Changes ◽  
High Fat ◽  
Low Fat Diet ◽  
Myocardial Degeneration ◽  
Lactating Females ◽  
Hydrogenated Soybean Oil

Severe degenerative myocardial disease occurred in female C3H/OUJ mice fed purified diets for 36 weeks; the diet contained 5% or 20% fat as non-hydrogenated soybean oil. Deaths of lactating females of this group (17/35 high fat diet and 7/35 low fat diet animals) were due to sudden cardiovascular collapse. Cardiomegaly with marked atrial and ventricular myocardial mineralization was seen at necropsy. Histologically. the random, myopathic foci were characterized by severe myocardial degeneration, mineralization, and fibrosis. Mural thrombosis, pulmonary arteriosclerosis, and mild myocardial inflammatory cell infiltrates were also present. Pathological changes were similar to those of dystrophic cardiac calcinosis, an incidental necropsy finding in certain mouse strains.

Temporal relation between neutrophil accumulation and myocardial reperfusion injury

1988 ◽  
Vol 255 (5) ◽  
pp. H1060-H1068 ◽  
Author(s):  
E. F. Smith ◽  
J. W. Egan ◽  
P. J. Bugelski ◽  
L. M. Hillegass ◽  
D. E. Hill ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Reperfusion Injury ◽  
Time Course ◽  
Myocardial Injury ◽  
Inflammatory Cells ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Neutrophil Accumulation ◽  
Cell Responses ◽  
Significant Linear Correlation

Infiltration of polymorphonuclear leukocytes (PMN) is associated with the progression of myocardial infarction and reperfusion injury. However, little is known about the time course of cellular infiltration. To investigate this issue, rats were subjected to 30 min of coronary artery occlusion followed by reperfusion for less than or equal to 96 h. Myocardial injury was determined by measuring the depletion of myocardial creatine phosphokinase activity, and PMN infiltration was assessed by measuring myeloperoxidase (MPO) activity. MPO activity increased from 0.7 U/g tissue in non-operated animals, to a peak of 6.7 +/- 0.8 and 6.4 +/- 1.4 U/g at 6 and 24 h after coronary artery reperfusion, respectively. MPO activity decreased to 3.3 +/- 0.8 U/g at 48 h and 1.1 +/- 0.4 U/g at 96 h, suggesting diminished PMN accumulation. Histological examination confirmed the accumulation and resolution of PMN over the 96-h period. At 24 h, there was a significant linear correlation between infarct size and MPO activity, whereas at 96 h no relationship was found. These data indicate that PMN infiltration occurs early in response to reperfusion injury and persists for only 24 h after initiation of reperfusion. These findings suggest that attempts to moderate inflammatory cell responses to myocardial injury should be administered early after coronary artery reperfusion to limit the accumulation of potentially deleterious inflammatory cells.

scholarly journals Anti-C5a complementary peptide mitigates zymosan-induced severe peritonitis with fibrotic encapsulation in rats pretreated with methylglyoxal

2018 ◽  
Vol 315 (6) ◽  
pp. F1732-F1746 ◽  
Author(s):  
Daiki Iguchi ◽  
Masashi Mizuno ◽  
Yasuhiro Suzuki ◽  
Fumiko Sakata ◽  
Shoichi Maruyama ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Subsequent Development ◽  
Inflammatory Cells ◽  
Therapeutic Effects ◽  
Pathological Changes ◽  
Dialysis Patients ◽  
Visceral Peritoneum ◽  
Peritoneal Encapsulation ◽  
Severe Peritonitis

In a previous study of fungal peritoneal injury in peritoneal dialysis patients, complement (C)-dependent pathological changes were developed in zymosan (Zy)-induced peritonitis by peritoneal scraping. However, the injuries were limited to the parietal peritoneum and did not show any fibrous encapsulation of the visceral peritoneum, which differs from human encapsular peritoneal sclerosis (EPS). We investigated peritoneal injury in a rat model of Zy-induced peritonitis pretreated with methylglyoxal (MGO) instead of scraping (Zy/MGO peritonitis) to clarify the role of C in the process of fibrous encapsulation of the visceral peritoneum. Therapeutic effects of an anti-C5a complementary peptide, AcPepA, on peritonitis were also studied. In Zy/MGO peritonitis, peritoneal thickness, fibrin exudation, accumulation of inflammatory cells, and deposition of C3b and C5b-9 with loss of membrane C regulators were increased along the peritoneum until day 5. On day 14, fibrous encapsulation of the visceral peritoneum was observed, resembling human EPS. Peritoneal injuries and fibrous changes were significantly improved with AcPepA treatment, even when AcPepA was administered following injection of Zy in Zy/MGO peritonitis. The data show that C5a might play a role in the development of encapsulation-like changes in the visceral peritoneum in Zy/MGO peritonitis. AcPepA might have therapeutic effects in fungal infection-induced peritoneal injury by preventing subsequent development of peritoneal encapsulation.

scholarly journals Evaluation of wound healing activity of alpha mangostin ointment in rats

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 1080-1087
Author(s):  
Sasikala Chinnappan ◽  
Venkatalakshmi Ranganathan ◽  
Jithendra Panneerselvam ◽  
Barani Karikalan ◽  
Thivashini vasanthan ◽  
...  
Keyword(s):  
Wound Healing ◽  
Wound Care ◽  
Inflammatory Cells ◽  
Treated Group ◽  
Wound Model ◽  
Wound Size ◽  
Group I ◽  
Significant Difference ◽  
Histopathological Studies ◽  
Wound Healing Activity

This study was aimed to evaluate the wound healing effects of alpha mangostin ointment using excision wound model. Twenty rats were divided into four groups of five rats each; group I was treated with ointment base (control), whereas group II, group III and group IV were treated with 10% (w/w) povidone-iodine (standard), alpha mangostin 1% (w/w), and alpha mangostin 2 % (w/w) respectively for wound healing evaluations. The size of the wound area was measured, and the reduction in the wound size was calculated, and the tissues examined histologically. The significant difference in the wound size reduction between the control and treated group (p<0.05) was observed in wound healing activity. Histopathological studies showed a lesser number of chronic inflammatory cells, lesser oedema and increased collagenisation in the test than control. This study showed that the alpha mangostin topical ointment could be a promising candidate for the betterment of wound care.

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