Lysozyme binding to endocardial endothelium mediates myocardial depression by the nitric oxide guanosine 3′,5′ monophosphate pathway in sepsis

Mink, Steven N.; Bose, Ratna; Roberts, Diane E.; Jacobs, Hans; Duke, Krika; Böse, Dirk; Cheng, Zhao-Qin; Light, R. Bruce

doi:10.1016/j.yjmcc.2005.06.009

Cited by 18 publications

(29 citation statements)

References 32 publications

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“…Moreover, we found that, in addition to reducing steady-state (SS) contraction, Lzm-S attenuated the response to field stimulation (FSR) in a canine right ventricular trabecular (RVT) preparation in which the sympathetic and parasympathetic nerves were stimulated (28). In subsequent experiments, we demonstrated that the mechanism by which Lzm-S decreased SS depression was mediated by nitric oxide (NO) release (27). We showed that Lzm-S interacted with the cardiac endothelium by binding to an N-glycoprotein to cause the release of NO (18,27).…”

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confidence: 95%

“…We showed that Lzm-S interacted with the cardiac endothelium by binding to an N-glycoprotein to cause the release of NO (18,27). NO then diffused to adjacent myocytes to activate the NO-cGMP pathway, which, in turn, led to myocardial depression (27).…”

mentioning

confidence: 96%

“…In subsequent experiments, we demonstrated that the mechanism by which Lzm-S decreased SS depression was mediated by nitric oxide (NO) release (27). We showed that Lzm-S interacted with the cardiac endothelium by binding to an N-glycoprotein to cause the release of NO (18,27). NO then diffused to adjacent myocytes to activate the NO-cGMP pathway, which, in turn, led to myocardial depression (27).…”

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confidence: 99%

“…Among the physiological compensatory mechanisms that would potentially limit loss of cardiac function in this condition, stimulation of the cardiac sympathetic neurons, which leads to an increase in the release of norepinephrine (NE), would be expected to be important. In a previous study, we used pore filtration and mass spectroscopymass spectroscopy (MS) sequencing (MS-MS) to identify a myocardial depressant factor that developed after Escherichia coli infusion in a canine model of septic shock (18,(27)(28)(29). We found that the inflammatory mediator lysozyme (Lzm-S), released from neutrophils and macrophages (5,10,16), contributed to the development of myocardial dysfunction in this model.…”

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confidence: 99%

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Lysozyme, a mediator of sepsis, impairs the cardiac neural adrenergic response by nonendothelial release of NO and inhibitory G protein signaling

Mink

Cheng²,

Bose³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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We previously showed that lysozyme (Lzm-S), derived from leukocytes, caused myocardial depression in canine sepsis by binding to the endocardial endothelium to release nitric oxide (NO). NO then diffuses to adjacent myocytes to activate the cGMP pathway. In a canine right ventricular trabecular (RVT) preparation, Lzm-S also decreased the inotropic response to field stimulation (FSR) during which the sympathetic and parasympathetic nerves were simulated to measure the adrenergic response. In the present study, we determined whether the pathway by which Lzm-S decreased FSR was different from the pathway by which Lzm-S reduced steady-state (SS) contraction. Furthermore, we determined whether the decrease in FSR was due to a decrease in sympathetic stimulation or enhanced parasympathetic signaling. In the RVT preparation, we found that the inhibitory effect of Lzm-S on FSR was prevented by NO synthase (NOS) inhibitors. A cGMP inhibitor also blocked the depressant activity of Lzm-S. However, in contrast to the Lzm-S-induced decline in SS contraction, chemical removal of the endocardial endothelium by Triton X-100 to eliminate endothelial NO release did not prevent the decrease in FSR. An inhibitory G protein was involved in the effect of Lzm-S, since FSR could be restored by treatment with pertussis toxin. Atropine prevented the Lzm-S-induced decline in FSR, whereas beta(1)- and beta(2)-adrenoceptor function was not impaired by Lzm-S. These results indicate that the Lzm-S-induced decrease in FSR results from a nonendothelial release of NO. NO then acts through inhibitory G protein to enhance parasympathetic signaling.

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confidence: 95%

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confidence: 96%

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confidence: 99%

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confidence: 99%

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Lysozyme, a mediator of sepsis, impairs the cardiac neural adrenergic response by nonendothelial release of NO and inhibitory G protein signaling

Mink

Cheng²,

Bose³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…La interacción endotelio-cardiomiocito es compleja durante la sepsis. El endotelio activado por la respuesta innata es capaz de producir NO, endotelina, prostaglandinas, entre otros compuestos capaces de interactuar y disminuir la capacidad contráctil del cardiomiocito en forma paracrina 40 . La activación de los cardiomiocitos, por su parte, favorece la permeabilidad endotelial y promueve la migración de leucocitos al intersticio 41 , que a su vez aumentan el daño inflamatorio local.…”

Section: Inflamaciónunclassified

Disfunción miocárdica en la sepsis

Andresen

Regueira

2010

Rev. méd. Chile

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The enigmatic function of IgD: some answers at last

2018

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IgD emerged soon after IgM at the time of inception of the adaptive immune system. Despite its evolutionary conservation from fish to humans, the specific functions of IgD have only recently begun to be elucidated. Mature B cells undergo alternative mRNA splicing to express IgD and IgM receptors with identical antigenic specificity. The enigma of dual IgD and IgM expression has been tackled by several recent studies showing that IgD helps peripheral accumulation of physiologically autoreactive B cells through its functional unresponsiveness to self-antigens but prompt readiness against foreign antigens. IgD achieves this balance by attenuating IgM-mediated anergy while promoting specific responses to multimeric non-self-antigens. Additional research has clarified how and why certain mucosal B cells become plasmablasts or plasma cells specializing in IgD secretion. In particular, the microbiota has been shown to play an important role in driving class switch-mediated replacement of IgM with IgD. Secreted IgD appears to enhance mucosal homeostasis and immune surveillance by "arming" myeloid effector cells such as basophils and mast cells with IgD antibodies reactive against mucosal antigens, including commensal and pathogenic microbes. Here we will review these advances and discuss their implications in humoral immunity in human and mice.

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Lysozyme binding to endocardial endothelium mediates myocardial depression by the nitric oxide guanosine 3′,5′ monophosphate pathway in sepsis

Cited by 18 publications

References 32 publications

Lysozyme, a mediator of sepsis, impairs the cardiac neural adrenergic response by nonendothelial release of NO and inhibitory G protein signaling

Lysozyme, a mediator of sepsis, impairs the cardiac neural adrenergic response by nonendothelial release of NO and inhibitory G protein signaling

Disfunción miocárdica en la sepsis

The enigmatic function of IgD: some answers at last

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