The cardiovascular influence of interleukin-1β on the expression of bradykinin B1 and B2 receptors

Riad, Alexander; Walther, Thomas; Yang, James; Altmann, Christine; Escher, Felicitas; Westermann, Dirk; Spillmann, Frank; Schultheiss, Heinz‐Peter; Tschöpe, Carsten

doi:10.1016/j.intimp.2007.07.027

International Immunopharmacology

2008

DOI: 10.1016/j.intimp.2007.07.027

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The cardiovascular influence of interleukin-1β on the expression of bradykinin B1 and B2 receptors

Alexander Riad

Thomas Walther

James Yang

et al.

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Cited by 8 publications

(1 citation statement)

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“…They are localized subcellulary either on the cell surface or in intracellular vesicular compartments (10). Although TLRs are expressed at low levels in a large number of cells, including nonimmune cells, the highest expression is generally on immune cells such as macrophages or lymphocytes, indicating a critical role of TLRs in function of those cells, including cytokine production (11). In the case of TLR4, this receptor has been demonstrated to modulate virus load and cardiac function in viral myocarditis (12,13).…”

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confidence: 99%

TRIF Is a Critical Survival Factor in Viral Cardiomyopathy

Riad

Westermann

Zietsch

et al. 2011

The Journal of Immunology

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TRIF is a member of the innate immune system known to be involved in viral recognition and type I IFN activation. Because IFNs are thought to play an important role in viral myocarditis, we investigated the role of TRIF in induced myocarditis in mice. Whereas C57BL/6 (wild-type) mice showed only mild myocarditis, including normal survival postinfection with coxsackievirus group B serotype 3 (CVB3), infection of TRIF−/− mice led to the induction of cardiac remodeling, severe heart failure, and 100% mortality (p < 0.0001). These mice showed markedly reduced virus control in cardiac tissues and cardiomyocytes. This was accompained with dynamic cardiac cytokine activation in the heart, including a suppression of the antiviral cytokine IFN-β in the early viremic phase. TRIF−/− myocytes displayed a TLR4-dependent suppression of IFN-β, and pharmacological treatment of CVB3-infected TRIF−/− mice with murine IFN-β led to improved virus control and reduced cardiac inflammation. Additionally, this treatment within the viremic phase of myocarditis showed a significant long-term outcome indexed by reduced mortality (20 versus 100%; p < 0.001). TRIF is essential toward a cardioprotection against CVB3 infection.

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confidence: 99%

TRIF Is a Critical Survival Factor in Viral Cardiomyopathy

Riad

Westermann

Zietsch

et al. 2011

The Journal of Immunology

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Hypoxic remodelling of Ca2+ stores does not alter human cardiac myofibroblast invasion

Riches

Hettiarachchi

Porter

et al. 2010

Biochemical and Biophysical Research Communications

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Dexmedetomidine protects the heart against ischemia reperfusion injury via regulation of the bradykinin receptors

Song

Tan

et al. 2021

European Journal of Pharmacology

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The cardiovascular influence of interleukin-1β on the expression of bradykinin B1 and B2 receptors

Cited by 8 publications

References 23 publications

TRIF Is a Critical Survival Factor in Viral Cardiomyopathy

TRIF Is a Critical Survival Factor in Viral Cardiomyopathy

Hypoxic remodelling of Ca2+ stores does not alter human cardiac myofibroblast invasion

Dexmedetomidine protects the heart against ischemia reperfusion injury via regulation of the bradykinin receptors

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