T lymphocytes from T. cruzi-infected mice alter heart contractility: Participation of arachidonic acid metabolites

Gorelik, Gabriela; Borda, Enri; Postan, Miriam; Cappa, Stella Gonzalez; Sterin‐Borda, Leonor

doi:10.1016/0022-2828(92)91155-x

Cited by 18 publications

(10 citation statements)

References 26 publications

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“…PKC activity was purified from subcellular fractions as previously described [21]; and was assayed on both cytosolic and membrane preparations from atria. The PKC substrate peptide, MBP (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14) from Life Technologies (Rochester, NY, USA) was used for measuring PKC activity purified from subcellular cardiac fractions, following the instructions of the PKC assay system of Life Technologies. PKC specificity was confirmed by means of the PKC pseudosubstrate inhibitor peptide PKC provided by Gibco (Calbad, CA, USA) [21].…”

Section: Protein Kinase C (Pkc) Activity Assaymentioning

confidence: 99%

“…Our research has been based on the hypothesis that cell-cell and antibody-cell interactions, mediated through neurotransmitter receptors of myocardial fibers and immune competent cell, determine the genesis and evolution of myocarditis. It is our belief that antisarcolemmal antibodies and lymphocytes interacting with β-adrenergic and muscarinic cholinergic receptors (mAChR) trigger molecular alterations, inexorably leading to cardiac damage [7,10,11]. Moreover, the presence of serum antibodies against the second extracellular loop of human M 2 mAChR are associated with chagasic dysautonomic syndrome [8,[12][13][14].…”

Section: Introductionmentioning

confidence: 99%

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Chagasic antibodies induce cardiac COX-2/iNOS mRNA expression with PGE2/NO production

Ganzinelli

Borda

Joensen

et al. 2009

International Journal of Cardiology

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Section: Protein Kinase C (Pkc) Activity Assaymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chagasic antibodies induce cardiac COX-2/iNOS mRNA expression with PGE2/NO production

Ganzinelli

Borda

Joensen

et al. 2009

International Journal of Cardiology

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“…This effect is blocked by cyclooxygenase inhibitors and has therefore been linked to the production of prostaglandin E2 [23]. Both infective microbial agents and inflammatory cells contribute to myocytolysis.…”

Section: Experimental Studiesmentioning

confidence: 99%

Autoimmunity in dilated cardiomyopathy

et al. 1996

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“…Most cytotoxic effects of lymphocytes are mediated by CD8 ÷ CTL or NK cells, although under certain circumstances CD4 + cells may also be cytotoxic [15]. It has been shown that T lymphocytes from Trypanosoma cruzi-infected mice can depress cardiac contractility [16]. In addition, Hassin et al [17] demonstrated that physiologic changes in contraction of cultured rat cardiac myocytes infected with Mingo virus could be induced by lymphocytes sensitized to Mingo virus.…”

Section: Effects Of Lymphocytes On Cardiac Myocytesmentioning

confidence: 99%

mentioning

confidence: 99%

Effects of cellular elements of the immune response on myocyte function and survival

Barry

1996

Heart Failure Rev

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The immune response is known to be associated with abnormalities of systolic and diastolic cardiac function during cardiac transplant rejection [1-3] and myocarditis [4]. In addition, autoimmunity may be an important contributor to depressed function in idiopathic dilated cardiomyopathy [5,6]. This immune response may impair cardiac performance by altering the function of individual myocytes, by causing myocyte necrosis and thus reducing the mass of functioning myocardium, or by a combination of these effects. The immune response consists of both cellular and humoral components. The cellular component can result in direct interaction of an inflammatory cell with the myocyte, or an indirect effect produced on the myocyte by virtue of secretion of soluble products such as cytokines by the inflammatory cell. The effects of cytokines on myocardial cells are considered at length in other articles in this issue. In this discussion we consider primarily the effects of direct interaction of various inflammatory cells participating in the immune response on myocyte function and survival. Components of the Cellular Inflammatory InfiltrateIt is first appropriate to consider the nature of the cellular infiltrate that occurs in an immune-mediated cardiac inflammation. Tilney and associates [7,8] showed that acutely rejecting cardiac rat allografts contain macrophages (15-25%), lymphocytes (75%), and neutrophils (5%). Of the lymphocytes, approximately 35% were B cells and the remainder were T lymphocytes. The initial infiltrate consists primarily of lymphocytes, with infiltration by a larger number of macrophages and neutrophils occurring with more complete rejection. Acute murine viral myocarditis is also associated with an infiltrate of macrophages and lymphocytes, including natural killer (NK) cells [9]. Recent work from our laboratory with the murine heterotopic mouse heart transplant model [10] demonstrated that the heart-infiltrating cell population consists of 44% lymphocytes, 30% macrophages, and 20% neutrophils 5-7 days after transplantation. Further studies in our laboratory have documented that the function of the transplanted heart is significantly depressed at this point [11]. We will therefore consider which components of this immune infiltrate could be responsible for cardiac depression during immune-mediated injury and the mechanisms involved. The work to be described will be focused primarily on the transplant rejection model, although, as mentioned earlier, it is very likely that similar mechanisms are involved in the myocardial functional depression noted during myocarditis, and possibly during autoimmune injury associated with idiopathic dilated cardiomyopathy. Effects of Lymphocytes on Cardiac MyocytesWe will first consider the effects oflymphocytes on myocyte function and survival. There are several types of lymphocytes that are involved in immune reactions. Cellular responses are mediated by T lymphocytes. Helper T lymphocytes (HTL; CD4 ÷) recognize endocytosed peptides that are bound to class II MHC mol...

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T lymphocytes from T. cruzi-infected mice alter heart contractility: Participation of arachidonic acid metabolites

Cited by 18 publications

References 26 publications

Chagasic antibodies induce cardiac COX-2/iNOS mRNA expression with PGE2/NO production

Chagasic antibodies induce cardiac COX-2/iNOS mRNA expression with PGE2/NO production

Autoimmunity in dilated cardiomyopathy

Effects of cellular elements of the immune response on myocyte function and survival

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