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Review

Trained Innate Immunity in Animal Models of Cardiovascular Diseases

by
Patricia Kleimann
1,
Lisa-Marie Irschfeld
2,
Maria Grandoch
3,4,
Ulrich Flögel
1,4 and
Sebastian Temme
4,5,*
1
Institute of Molecular Cardiology, Faculty of Medicine, University Hospital, Heinrich-Heine-University, 40225 Düsseldorf, Germany
2
Department of Radiation Oncology, Faculty of Medicine, University Hospital, Heinrich-Heine-University, 40225 Düsseldorf, Germany
3
Institute of Translational Pharmacology, Faculty of Medicine, University Hospital, Heinrich-Heine-University, 40225 Düsseldorf, Germany
4
Cardiovascular Research Institute Düsseldorf (CARID), University Hospital, 40225 Düsseldorf, Germany
5
Department of Anesthesiology, Faculty of Medicine, University Hospital, Heinrich-Heine-University, 40225 Düsseldorf, Germany
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2024, 25(4), 2312; https://doi.org/10.3390/ijms25042312
Submission received: 14 January 2024 / Revised: 11 February 2024 / Accepted: 12 February 2024 / Published: 15 February 2024

Abstract

Acquisition of immunological memory is an important evolutionary strategy that evolved to protect the host from repetitive challenges from infectious agents. It was believed for a long time that memory formation exclusively occurs in the adaptive part of the immune system with the formation of highly specific memory T cells and B cells. In the past 10–15 years, it has become clear that innate immune cells, such as monocytes, natural killer cells, or neutrophil granulocytes, also have the ability to generate some kind of memory. After the exposure of innate immune cells to certain stimuli, these cells develop an enhanced secondary response with increased cytokine secretion even after an encounter with an unrelated stimulus. This phenomenon has been termed trained innate immunity (TI) and is associated with epigenetic modifications (histone methylation, acetylation) and metabolic alterations (elevated glycolysis, lactate production). TI has been observed in tissue-resident or circulating immune cells but also in bone marrow progenitors. Risk-factors for cardiovascular diseases (CVDs) which are associated with low-grade inflammation, such as hyperglycemia, obesity, or high salt, can also induce TI with a profound impact on the development and progression of CVDs. In this review, we briefly describe basic mechanisms of TI and summarize animal studies which specifically focus on TI in the context of CVDs.
Keywords: trained innate immunity; cardiovascular diseases; monocytes; bone marrow; animal models trained innate immunity; cardiovascular diseases; monocytes; bone marrow; animal models

Share and Cite

MDPI and ACS Style

Kleimann, P.; Irschfeld, L.-M.; Grandoch, M.; Flögel, U.; Temme, S. Trained Innate Immunity in Animal Models of Cardiovascular Diseases. Int. J. Mol. Sci. 2024, 25, 2312. https://doi.org/10.3390/ijms25042312

AMA Style

Kleimann P, Irschfeld L-M, Grandoch M, Flögel U, Temme S. Trained Innate Immunity in Animal Models of Cardiovascular Diseases. International Journal of Molecular Sciences. 2024; 25(4):2312. https://doi.org/10.3390/ijms25042312

Chicago/Turabian Style

Kleimann, Patricia, Lisa-Marie Irschfeld, Maria Grandoch, Ulrich Flögel, and Sebastian Temme. 2024. "Trained Innate Immunity in Animal Models of Cardiovascular Diseases" International Journal of Molecular Sciences 25, no. 4: 2312. https://doi.org/10.3390/ijms25042312

APA Style

Kleimann, P., Irschfeld, L.-M., Grandoch, M., Flögel, U., & Temme, S. (2024). Trained Innate Immunity in Animal Models of Cardiovascular Diseases. International Journal of Molecular Sciences, 25(4), 2312. https://doi.org/10.3390/ijms25042312

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