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      Resolution of inflammation: an integrated view

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          Abstract

          Resolution of inflammation is a coordinated and active process aimed at restoration of tissue integrity and function. This review integrates the key molecular and cellular mechanisms of resolution. We describe how abrogation of chemokine signalling blocks continued neutrophil tissue infiltration and how apoptotic neutrophils attract monocytes and macrophages to induce their clearance. Uptake of apoptotic neutrophils by macrophages reprograms macrophages towards a resolving phenotype, a key event to restore tissue homeostasis. Finally, we highlight the therapeutic potential that derives from understanding the mechanisms of resolution.

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          Transcriptional profiling of the human monocyte-to-macrophage differentiation and polarization: new molecules and patterns of gene expression.

          Alberto Mantovani, Laurent Martinez, Massimo Locati … (2006)
          Comprehensive analysis of the gene expression profiles associated with human monocyte-to-macrophage differentiation and polarization toward M1 or M2 phenotypes led to the following main results: 1) M-CSF-driven monocyte-to-macrophage differentiation is associated with activation of cell cycle genes, substantiating the underestimated proliferation potential of monocytes. 2) M-CSF leads to expression of a substantial part of the M2 transcriptome, suggesting that under homeostatic conditions a default shift toward M2 occurs. 3) Modulation of genes involved in metabolic activities is a prominent feature of macrophage differentiation and polarization. 4) Lipid metabolism is a main category of modulated transcripts, with expected up-regulation of cyclo-oxygenase 2 in M1 cells and unexpected cyclo-oxygenase 1 up-regulation in M2 cells. 5) Each step is characterized by a different repertoire of G protein-coupled receptors, with five nucleotide receptors as novel M2-associated genes. 6) The chemokinome of polarized macrophages is profoundly diverse and new differentially expressed chemokines are reported. Thus, transcriptome profiling reveals novel molecules and signatures associated with human monocyte-to-macrophage differentiation and polarized activation which may represent candidate targets in pathophysiology.
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            In vivo labeling with 2H2O reveals a human neutrophil lifespan of 5.4 days.

            Janesh Pillay, Ineke den Braber, Nienke Vrisekoop … (2010)
            Neutrophils are essential effector cells of the innate immune response and are indispensable for host defense. Apart from their antimicrobial functions, neutrophils inform and shape subsequent immunity. This immune modulatory functionality might however be considered limited because of their generally accepted short lifespan (< 1 day). In contrast to the previously reported short lifespans acquired by ex vivo labeling or manipulation, we show that in vivo labeling in humans with the use of (2)H(2)O under homeostatic conditions showed an average circulatory neutrophil lifespan of 5.4 days. This lifespan is at least 10 times longer than previously reported and might lead to reappraisal of novel neutrophil functions in health and disease.
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              Annexin A1 and glucocorticoids as effectors of the resolution of inflammation.

              Mauro Perretti, Fulvio D'Acquisto (2009)
              Glucocorticoids are widely used for the management of inflammatory diseases. Their clinical application stems from our understanding of the inhibitory effect of the corticosteroid hormone cortisol on several components of the immune system. Endogenous and exogenous glucocorticoids mediate their multiple anti-inflammatory effects through many effector molecules. In this Opinion article, we focus on the role of one such effector molecule, annexin A1, and summarize the recent studies that provide insight into its molecular and pharmacological functions in immune responses. In addition, we propose a model in which glucocorticoids regulate the expression and function of annexin A1 in opposing ways in innate and adaptive immune cells to mediate the resolution of inflammation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): EMBO Mol Med
                Journal ID (iso-abbrev): EMBO Mol Med
                Journal ID (publisher-id): emmm
                Title: EMBO Molecular Medicine
                Publisher: WILEY-VCH Verlag (Weinheim )
                ISSN (Print): 1757-4676
                ISSN (Electronic): 1757-4684
                Publication date (Print): May 2013
                Publication date (Electronic): 17 April 2013
                Volume: 5
                Issue: 5
                Pages: 661-674
                Affiliations
                [1 ]Institute for Cardiovascular Prevention, LMU Munich, Germany
                [2 ]William Harvey Research Institute, Barts and The London School of Medicine London, UK
                [3 ]Department of Pathology, AMC Amsterdam, The Netherlands
                Author notes
                * Corresponding author: Tel: +49 89 5160 4365; Fax: +49 89 5160 4352; E-mail: oliver.soehnlein@ 123456gmail.com
                Article
                DOI: 10.1002/emmm.201202382
                PMC ID: 3662311
                PubMed ID: 23592557
                SO-VID: f341d0d6-56b9-4508-aee6-a5511e05157b
                Copyright © Copyright © 2013 The Authors. Published by John Wiley and Sons, Ltd on behalf of EMBO
                License:

                This is an open access article under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 17 December 2012
                Date revision received : 22 February 2013
                Date accepted : 01 March 2013
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: apoptosis,efferocytosis,macrophage reprogramming,pro-resolving drugs,tissue homeostasis
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: apoptosis, efferocytosis, macrophage reprogramming, pro-resolving drugs, tissue homeostasis

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