3
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Biomarkers in Community-Acquired Pneumonia (Cardiac and Non-Cardiac)

      review-article
      1 , 2 , 4 , 1 , 2 , 3 , *
      Journal of Clinical Medicine
      MDPI
      pneumonia, biomarkers, cardiac, cardiovascular

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Community-acquired pneumonia (CAP) remains the first cause of morbidity and mortality worldwide due to infection. Several aspects such as severity and host response are related to its clinical course and outcome. Beyond the acute implications that the infection provokes in the host, pneumonia also has long-term negative consequences. Among them, cardiovascular complications and mortality are the most outstanding. Therefore, an adequate recognition and stratification of the risk of complications and mortality is crucial. Many biomarkers have been studied for these reasons, considering that each biomarker mirrors a different aspect. Moreover, the clinical application of many of them is still being deliberated because of their limitations and the heterogeneity of the disease. In this review, we examine some of the most relevant biomarkers that we have classified as cardiac and non-cardiac. We discuss some classic biomarkers and others that are considered novel biomarkers, which are mainly involved in cardiovascular risk.

          Related collections

          Most cited references107

          • Record: found
          • Abstract: found
          • Article: not found

          Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood.

          It has been known for many years that neutrophils and platelets participate in the pathogenesis of severe sepsis, but the inter-relationship between these players is completely unknown. We report several cellular events that led to enhanced trapping of bacteria in blood vessels: platelet TLR4 detected TLR4 ligands in blood and induced platelet binding to adherent neutrophils. This led to robust neutrophil activation and formation of neutrophil extracellular traps (NETs). Plasma from severely septic humans also induced TLR4-dependent platelet-neutrophil interactions, leading to the production of NETs. The NETs retained their integrity under flow conditions and ensnared bacteria within the vasculature. The entire event occurred primarily in the liver sinusoids and pulmonary capillaries, where NETs have the greatest capacity for bacterial trapping. We propose that platelet TLR4 is a threshold switch for this new bacterial trapping mechanism in severe sepsis.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            Neutrophil Extracellular Traps Directly Induce Epithelial and Endothelial Cell Death: A Predominant Role of Histones

            Neutrophils play an important role in innate immunity by defending the host organism against invading microorganisms. Antimicrobial activity of neutrophils is mediated by release of antimicrobial peptides, phagocytosis as well as formation of neutrophil extracellular traps (NET). These structures are composed of DNA, histones and granular proteins such as neutrophil elastase and myeloperoxidase. This study focused on the influence of NET on the host cell functions, particularly on human alveolar epithelial cells as the major cells responsible for gas exchange in the lung. Upon direct interaction with epithelial and endothelial cells, NET induced cytotoxic effects in a dose-dependent manner, and digestion of DNA in NET did not change NET-mediated cytotoxicity. Pre-incubation of NET with antibodies against histones, with polysialic acid or with myeloperoxidase inhibitor but not with elastase inhibitor reduced NET-mediated cytotoxicity, suggesting that histones and myeloperoxidase are responsible for NET-mediated cytotoxicity. Although activated protein C (APC) did decrease the histone-induced cytotoxicity in a purified system, it did not change NET-induced cytotoxicity, indicating that histone-dependent cytotoxicity of NET is protected against APC degradation. Moreover, in LPS-induced acute lung injury mouse model, NET formation was documented in the lung tissue as well as in the bronchoalveolar lavage fluid. These data reveal the important role of protein components in NET, particularly histones, which may lead to host cell cytotoxicity and may be involved in lung tissue destruction.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              NETosis: how vital is it?

              In this review, we examine the evidence that neutrophil extracellular traps (NETs) play a critical role in innate immunity. We summarize how NETs are formed in response to various stimuli and provide evidence that NETosis is not universally a cell death pathway. Here we describe at least 2 different mechanisms by which NETs are formed, including a suicide lytic NETosis and a live cell or vital NETosis. We also evaluate the evidence for NETs in catching and killing pathogens. Finally, we examine how infections are related to the development of autoimmune and vasculitic diseases through unintended but detrimental bystander damage resulting from NET release.
                Bookmark

                Author and article information

                Journal
                J Clin Med
                J Clin Med
                jcm
                Journal of Clinical Medicine
                MDPI
                2077-0383
                18 February 2020
                February 2020
                : 9
                : 2
                : 549
                Affiliations
                [1 ]Pneumology Department, Hospital Universitario y Politécnico La Fe/Instituto de Investigación Sanitaria (IIS) La Fe, 46026 Valencia, Spain; Pneumology Department, Hospital Universitario y Politécnico La Fe, Avda, Fernando Abril Martorell 106, 46026 Valencia, Spain; rmendezalcoy@ 123456gmail.com
                [2 ]University of Valencia, Medicine Faculty, 46026 Valencia, Spain; irene.aldas.criado@ 123456gmail.com
                [3 ]Centro de Investigación Biomédica en Red Enfermedades Respiratorias (CIBERES), 28029 Madrid, Spain
                [4 ]Pneumology Department, Hospital Germans Trias i Pujol, 08916 Badalona, Spain
                Author notes
                [* ]Correspondence: rosmenend@ 123456gmail.com
                Author information
                https://orcid.org/0000-0001-6300-9836
                https://orcid.org/0000-0001-9291-873X
                Article
                jcm-09-00549
                10.3390/jcm9020549
                7073979
                32085380
                03fdf415-02d8-4a74-96f4-bb5111f64f8e
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 07 January 2020
                : 10 February 2020
                Categories
                Review

                pneumonia,biomarkers,cardiac,cardiovascular
                pneumonia, biomarkers, cardiac, cardiovascular

                Comments

                Comment on this article