Survival and Cardiac Remodeling after Myocardial Infarction Are Critically Dependent on the Host Innate Immune Interleukin-1 Receptor Associated Kinase-4 (IRAK-4) Signaling: A Regulator of Bone Marrow-Derived Dendritic Cells

Maekawa, Yuichiro; Mizue, Nobuo; Chan, Annie W.; Yu, Shuang; Liu, Youan; Chen, Manyin; Dawood, Fayez; Coute, Geoffrey de; Li, Guo Hua; Medin, Jeffrey A.

doi:10.1016/j.cardfail.2009.06.430

Cited by 18 publications

(27 citation statements)

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“…Following antigen contact, they maturate in regional lymph nodes, and induce T‐cell differentiation and proliferation. Such an inflammatory role for mDCs has also been described in myocardial tissue following acute myocardial infarction, as they seem to contribute greatly to T‐cell activation that leads to tissue remodelling and deterioration of ventricular function . While circulatory DC precursors, as well as other immune cells are reduced in peripheral blood of humans in the event of an acute myocardial infarction,, our study group recently found out that such peripheral reduction was due to an increased infiltration of DCs, T cells, and macrophages in human infarcted myocardial tissue .…”

Section: Discussionsupporting

confidence: 55%

Decrease in dendritic cells in endomyocardial biopsies of human dilated cardiomyopathy

Pistulli

König

Drobnik

et al. 2013

European J of Heart Fail

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Aims Dendritic cells (DCs) are sentinels of the immune system—their role in myocardial disease is unknown as yet. We investigated their myocardial presence in human dilated cardiomyopathy (DCM). Methods and results Endomyocardial biopsies from 72 patients with DCM (EF ∼30%), as well as myocardial specimens from 18 suicide or accident victims were immunohistochemically analysed for myeloid and plasmacytoid DCs, antigen‐presenting cells (APCs), and other leucocytes; also tissue fibrosis and apoptosis were histologically quantified. The myocardial viral genome was identified through polymerase chain reaction, and patients underwent clinical follow‐up in 3–6 months. We found myocardial DCs of all examined subtypes and maturation stages (fascin, CD11c, CD209, CD83, and CD304), as well as markers for APCs (HLA‐DR and CD40) and T‐cell activation (CD69) to be significantly decreased in DCM compared with controls. In contrast, regulatory T cells (the GITR epitope), apoptosis (by TUNEL reaction and immunostaining with BCL‐2), and a DC chemokine receptor (CCR7) were overexpressed, while no significant differences were observed for macrophages (CD68). Immature myeloid and plasmacytoid DCs strongly correlated with endothelial progenitor cells (CD34), which were similarly reduced in DCM, and inversely correlated with fibrosis. Myeloid DCs were especially reduced in virus‐positive biopsies, and their numbers correlated with positive change in EF (ΔEF) at follow‐up. Conclusion Myocardial DCs are reduced in heart biopsies of symptomatic DCM patients. Such a reduction correlates with an unfavourable short‐term outcome in terms of EF, and could result from myocardial tissue damage, cellular death, and insufficient vascularization in chronic heart failure.

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Section: Discussionsupporting

confidence: 55%

Decrease in dendritic cells in endomyocardial biopsies of human dilated cardiomyopathy

Pistulli

König

Drobnik

et al. 2013

European J of Heart Fail

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“…The reason for this is not known at this time. The timing for the judgement might be not adequate for split of surviving rates, because the clue arose indicating the death rate was increased in later time of myocardial infarction [40,41].…”

Section: Discussionmentioning

confidence: 99%

Degeneration of capsaicin sensitive sensory nerves enhances myocardial injury in acute myocardial infarction in rats

Zhang

Guo

Wang

et al. 2012

International Journal of Cardiology

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“…In the blood, both subtypes of DC are found as circulating DC precursors that lack the expression of costimulatory molecules, so that they are unable to activate other inflammatory cells. In the infarcted myocardium, it was reported that mDC became activated in response to danger signals such as heat shock protein, which is released from necrotic tissue after MI, through the activation of toll‐like receptors (TLRs) signaling …”

Section: Discussionmentioning

confidence: 99%

Decreased Myocardial Dendritic Cells is Associated With Impaired Reparative Fibrosis and Development of Cardiac Rupture After Myocardial Infarction in Humans

Nagai

Honda

Sugano

et al. 2014

JAHA

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BackgroundDendritic cells (DC) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the infarcted heart and its immunoprotective roles in the post‐infarction healing process after experimental myocardial infarction (MI). However, its clinical significance has not been determined.Methods and ResultsThe degree of DC infiltration and its correlation with the post‐infarction healing process in the human infarcted heart were investigated in 24 autopsy subjects after ST‐elevation MI. Patients were divided into two groups according to the presence (n=13) or absence (n=11) of cardiac rupture. The numbers of infiltrated DC and macrophages and the extent of fibrosis in the infarcted area were examined. In the rupture group, CD68+ macrophage infiltration was increased and CD209+ DC, and CD11c+ DC infiltration and the extent of reparative fibrosis were decreased compared with the non‐rupture group, under matched baseline characteristics including the time from onset to death and use of revascularization. Furthermore, there was a significant positive correlation between the number of infiltrating CD209+ DC, and CD11c+ DC and the extent of reparative fibrosis.ConclusionsDecreased number of DC in human‐infarcted myocardial tissue was associated with increased macrophage infiltration, impaired reparative fibrosis, and the development of cardiac rupture after MI. These findings suggest a protective role of DC in post‐MI inflammation and the subsequent healing process.

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Survival and Cardiac Remodeling after Myocardial Infarction Are Critically Dependent on the Host Innate Immune Interleukin-1 Receptor Associated Kinase-4 (IRAK-4) Signaling: A Regulator of Bone Marrow-Derived Dendritic Cells

Cited by 18 publications

References 0 publications

Decrease in dendritic cells in endomyocardial biopsies of human dilated cardiomyopathy

Decrease in dendritic cells in endomyocardial biopsies of human dilated cardiomyopathy

Degeneration of capsaicin sensitive sensory nerves enhances myocardial injury in acute myocardial infarction in rats

Decreased Myocardial Dendritic Cells is Associated With Impaired Reparative Fibrosis and Development of Cardiac Rupture After Myocardial Infarction in Humans

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