Characteristics of the Cardiosplenic Axis in Patients with Fatal Myocardial Infarction

Kercheva, M. A.; Ryabov, V. V.; Trusov, A. A.; Stepanov, Ivan; Kzhyshkowska, Julia

doi:10.3390/life12050673

Cited by 3 publications

(4 citation statements)

References 28 publications

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“…Ismahil et al then found that splenectomy post-MI reduces adverse cardiac remodeling, while the adoptive transfer of splenocytes from mice with ischemic heart failure is sufficient to produce adverse cardiac remodeling in naïve mice (16). Consistent with these findings, autopsies of patients with fatal MI revealed an accumulation of monocytes at the infarcted myocardium with concurrent monocyte depletion in the spleen (25,26). In another study of 22 patients with ischemic MI, fludeoxyglucose-18 (FDG) positron emission tomography (PET) revealed increased splenic inflammation post-MI relative to control patients (27).…”

Section: Discussionmentioning

confidence: 88%

B cell-mediated antigen presentation promotes adverse cardiac remodeling in chronic heart failure

Lovell,

Duque,

Rousseau

et al. 2024

Preprint

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Cardiovascular disease remains the leading cause of death worldwide. A primary driver of cardiovascular mortality is ischemic heart failure, a form of cardiac dysfunction that develops in patients who survive myocardial infarction. Acute cardiac damage triggers robust changes in the spleen with rapid migration of immune cells from the spleen to the heart. Activating this cardio-splenic axis contributes to progressive cardiac dysfunction. The cardio-splenic axis has, therefore, been identified as a promising therapeutic target to prevent or treat heart failure. However, our understanding of the precise mechanisms by which specific immune cells contribute to adverse cardiac remodeling within the cardio-splenic axis remains limited. Here, we show that splenic B cells contribute to the development of heart failure via MHC II-mediated antigen presentation. We found that the transfer of splenic B cells from mice with ischemic heart failure promoted adverse cardiac remodeling and splenic inflammatory changes in naive recipient mice. Based on single-cell RNA sequencing analysis of splenic B cells from mice with ischemic heart failure, we hypothesized that B cells contributed to adverse cardiac remodeling through antigen presentation by MHC II molecules. This mechanism was confirmed using transgenic mice with B cell-specific MHC II deletion and by analyzing circulating B cells from humans who experienced myocardial infarction. Our results broaden our understanding of B lymphocyte biology, reshape current models of immune activation in response to cardiac injury, and point towards MHC II-mediated signaling in B cells as a novel and specific therapeutic target in chronic heart failure.

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Section: Discussionmentioning

confidence: 88%

B cell-mediated antigen presentation promotes adverse cardiac remodeling in chronic heart failure

Lovell,

Duque,

Rousseau

et al. 2024

Preprint

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“…Однако возможно, что для лиц без ССЗ сниженный генез данного фенотипа клеток служит вариантом физиологической нормы, и, напротив, у лиц с ИМ недостаточный генез данного типа клеток с противовоспалительной активностью может обусловливать неблагоприятный исход, что подтверждают ранее полученные экспериментальные данные о полезной роли репаративных мф на ранней стадии воспаления и связи дефицита CD206+ в миокарде с фатальным исходом [12]. Низкое содержание данного фенотипа клеток при ИМ в КП наряду с их низким содержанием в БП может отражать истощение дан-ного типа клеток или их недостаточную выработку, что может обусловливать неблагоприятный исход [3,10]. Однако, согласно полученным ранее данным, не складывается однозначного впечатления о благоприятном или, напротив, негативном влиянии пониженного/повышенного содержания CD206+ клеток на процессы регенерации миокарда и клинические исходы в условиях острой ишемии миокарда [3,12,16].…”

Section: Discussionunclassified

“…ранее комплексное сопоставление количественного содержания спектра мф, включающих как мф М1, так и М2 типа, не проводилось ни в эксперименте, ни в клинике; не сравнивалось их содержание между лицами с ИМ и контрольной группой. Существующие ранее экспериментальные данные оценивали содержание либо одного из фенотипов мф в эксперименте [5], либо содержание предшественников мф -моноцитов [10].…”

Section: Discussionunclassified

Place of the cardiosplenic axis in the development of fatal myocardial infarction

et al. 2023

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Aim. To compare data on the features of spleen macrophage composition in patients with fatal myocardial infarction (MI) and in patients from the control group without cardiovascular disease (CVD).Material and methods. The study included patients with fatal MI (n=30) and control group (n=5) — persons without CVD who died from injuries not compatible with life. Macrophage infiltration of spleen and myocardium fragments taken during autopsy was assessed by immunohistochemistry using macrophage markers CD68, CD163, CD206, stabilin-1.Results. There were following number of cells studied by us in the red pulp (RP) in patients with MI: CD163+, 906 (661; 1101), CD68+, 898 (807; 1049), stabilin-1+, 811 (531; 966), CD206+, 11 (9; 19); control group: CD163+, 400 (315; 513), CD68+, 40 (37; 45), stabilin-1+, 186 (107; 206), CD206+, 80 (70; 84). The content of all cells in the RP in patients with MI was high and prevailed over their number in the control group, while only the CD206+ concentration was inferior in number; in the control group, CD163+ cells predominated (p<0,05). There were following number of cells in the white pulp (WP): CD68+, 312 (260; 348), stabilin-1+, 59 (40; 123), CD163+, 29 (17; 56), CD206+, 2 (1; 5) in the group with MI; CD68+, 3 (1; 4), stabilin-1+, 3 (2; 3), CD163+, 23 (1; 48), CD206+, 1 (1; 2) in the control group. In persons with MI, CD68+ cells dominated in WP, while in the control group — CD163+ (p<0,05). The minimum and comparable in WP in both groups was the number of CD206+ cells (p<0,05), which correlated in the control group with the level of stabilin-1+ and CD206+ cells (r=-0,9, p=0,003) and in patients with MI — with the level of CD206+ cells in the myocardium (r=0,6, p=0,004).Conclusion. The dominance of CD163+ cells in all functional spleen areas in the control group and CD68+ cells in patients with MI was revealed. The only cell type, the content of which in the control group prevailed over that in MI in RP and correlated in WP with its myocardial concentration, was CD206+.

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“…The main clinical and anamnestic data of the study sample were reported in our studies into the morphometric characteristics of the spleen in patients with fatal MI [9]. The time from the onset of the disease to admission to the hospital was 180 min (120-720 min.).…”

Section: Clinical and Anamnestic Datamentioning

confidence: 99%

Macrophages of the cardiosplenal axis and their content in patients with myocardial infarction

Kercheva

Ryabov

Trusov

et al. 2023

SJCEM

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The spleen is one of the main reservoirs of monocytes, the leading cells of the post-infarction inflammatory response.Aim: To assess features of splenic macrophage infiltration, its dynamics and correlations with myocardial macrophage infiltration and an adverse course of the myocardial infarction (MI)Material and Methods. The macrophage composition of spleen and myocardium sections of patients (n = 30) with fatal MI and persons from the control group without cardiovascular disease (n = 5) was assessed by immunohistochemistry.Results and conclusion. All investigated cells, as CD68+, CD163+, CD206+, and stabilin-1+ were represented in the spleen regardless of the presence of MI. Their number in spleen in patients with MI remained consistently high regardless of the period of MI, and was accompanied by an increased number of such cells in the infarction area of myocardium. CD68+, CD163+ and stabilin-1+ cells predominated in the red pulp in patients with fatal MI, its number many fold exceeded that in the control group and that in the white pulp and in the infarction area of myocardium. In the white pulp of patients with fatal MI, the number of CD68+ cells predominated, in persons from the control group – CD163+. We revealed only one cell types whose content in the spleen in the control group was higher than in individuals with fatal MI – CD206+in the red pulp. Low content of CD206+ cells in the red and white pulp of the spleen characterized patients with a fatal outcome of MI.

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Characteristics of the Cardiosplenic Axis in Patients with Fatal Myocardial Infarction

Cited by 3 publications

References 28 publications

B cell-mediated antigen presentation promotes adverse cardiac remodeling in chronic heart failure

B cell-mediated antigen presentation promotes adverse cardiac remodeling in chronic heart failure

Place of the cardiosplenic axis in the development of fatal myocardial infarction

Macrophages of the cardiosplenal axis and their content in patients with myocardial infarction

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