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      Role of Inflammatory Cell Subtypes in Heart Failure

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          Abstract

          Inflammation is a well-known feature of heart failure. Studies have shown that while some inflammation is required for repair during injury and is protective, prolonged inflammation leads to myocardial remodeling and apoptosis of cardiac myocytes. Various types of immune cells are implicated in myocardial inflammation and include neutrophils, macrophages, eosinophils, mast cells, natural killer cells, T cells, and B cells. Recent clinical trials have targeted inflammatory cascades as therapy for heart failure with limited success. A better understanding of the temporal course of the infiltration of the different immune cells and their contribution to the inflammatory process may improve the success for therapy. This brief review outlines the major cell types involved in heart failure, and some of their actions are summarized in the supplementary figure.

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          The inflammatory response in myocardial injury, repair, and remodelling.

          Nikolaos G Frangogiannis (2014)
          Myocardial infarction triggers an intense inflammatory response that is essential for cardiac repair, but which is also implicated in the pathogenesis of postinfarction remodelling and heart failure. Signals in the infarcted myocardium activate toll-like receptor signalling, while complement activation and generation of reactive oxygen species induce cytokine and chemokine upregulation. Leukocytes recruited to the infarcted area, remove dead cells and matrix debris by phagocytosis, while preparing the area for scar formation. Timely repression of the inflammatory response is critical for effective healing, and is followed by activation of myofibroblasts that secrete matrix proteins in the infarcted area. Members of the transforming growth factor β family are critically involved in suppression of inflammation and activation of a profibrotic programme. Translation of these concepts to the clinic requires an understanding of the pathophysiological complexity and heterogeneity of postinfarction remodelling in patients with myocardial infarction. Individuals with an overactive and prolonged postinfarction inflammatory response might exhibit left ventricular dilatation and systolic dysfunction and might benefit from targeted anti-IL-1 or anti-chemokine therapies, whereas patients with an exaggerated fibrogenic reaction can develop heart failure with preserved ejection fraction and might require inhibition of the Smad3 (mothers against decapentaplegic homolog 3) cascade. Biomarker-based approaches are needed to identify patients with distinct pathophysiologic responses and to rationally implement inflammation-modulating strategies.
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            Immune cell regulation by autocrine purinergic signalling.

            Wolfgang Junger (2011)
            Stimulation of almost all mammalian cell types leads to the release of cellular ATP and autocrine feedback through a diverse array of purinergic receptors. Depending on the types of purinergic receptors that are involved, autocrine signalling can promote or inhibit cell activation and fine-tune functional responses. Recent work has shown that autocrine signalling is an important checkpoint in immune cell activation and allows immune cells to adjust their functional responses based on the extracellular cues provided by their environment. This Review focuses on the roles of autocrine purinergic signalling in the regulation of both innate and adaptive immune responses and discusses the potential of targeting purinergic receptors for treating immune-mediated disease.
            Article 0 comments Cited 274 times – based on 0 reviews     Review now
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              Emerging roles for platelets as immune and inflammatory cells.

              Craig Morrell, Angela A Aggrey, Lesley M Chapman … (2014)
              Despite their small size and anucleate status, platelets have diverse roles in vascular biology. Not only are platelets the cellular mediator of thrombosis, but platelets are also immune cells that initiate and accelerate many vascular inflammatory conditions. Platelets are linked to the pathogenesis of inflammatory diseases such as atherosclerosis, malaria infection, transplant rejection, and rheumatoid arthritis. In some contexts, platelet immune functions are protective, whereas in others platelets contribute to adverse inflammatory outcomes. In this review, we will discuss platelet and platelet-derived mediator interactions with the innate and acquired arms of the immune system and platelet-vessel wall interactions that drive inflammatory disease. There have been many recent publications indicating both important protective and adverse roles for platelets in infectious disease. Because of this new accumulating data, and the fact that infectious disease continues to be a leading cause of death globally, we will also focus on new and emerging concepts related to platelet immune and inflammatory functions in the context of infectious disease.
              Article 0 comments Cited 260 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Derek Strassheim:
                ORCID: https://orcid.org/0000-0001-5264-6792
                Journal
                Journal ID (nlm-ta): J Immunol Res
                Journal ID (iso-abbrev): J Immunol Res
                Journal ID (publisher-id): JIR
                Title: Journal of Immunology Research
                Publisher: Hindawi
                ISSN (Print): 2314-8861
                ISSN (Electronic): 2314-7156
                Publication date Collection: 2019
                Publication date (Electronic): 2 September 2019
                Volume: 2019
                Electronic Location Identifier: 2164017
                Affiliations
                1Cardiovascular Pulmonary Research Laboratory, University of Colorado Denver, Aurora CO, USA
                2Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Denver, Aurora CO, USA
                3Rocky Mountain Regional VA Medical Center, Aurora CO, USA
                4Department of Pediatrics, University of Colorado Denver, Aurora CO, USA
                Author notes

                Academic Editor: Ilaria Roato

                Author information
                https://orcid.org/0000-0001-5264-6792
                Article
                DOI: 10.1155/2019/2164017
                PMC ID: 6745095
                PubMed ID: 31565659
                SO-VID: 956677d1-3b44-4aae-a32b-87468c4c820d
                Copyright © Copyright © 2019 Derek Strassheim et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 20 December 2018
                Date accepted : 25 July 2019
                Categories
                Subject: Review Article

                Data availability:

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