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      Glucocorticoids Shape Macrophage Phenotype for Tissue Repair

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          Abstract

          Inflammation is a complex process which is highly conserved among species. Inflammation occurs in response to injury, infection, and cancer, as an allostatic mechanism to return the tissue and to return the organism back to health and homeostasis. Excessive, or chronic inflammation is associated with numerous diseases, and thus strategies to combat run-away inflammation is required. Anti-inflammatory drugs were therefore developed to switch inflammation off. However, the inflammatory response may be beneficial for the organism, in particular in the case of sterile tissue injury. The inflammatory response can be divided into several parts. The first step is the mounting of the inflammatory reaction itself, characterized by the presence of pro-inflammatory cytokines, and the infiltration of immune cells into the injured area. The second step is the resolution phase, where immune cells move toward an anti-inflammatory phenotype and decrease the secretion of pro-inflammatory cytokines. The last stage of inflammation is the regeneration process, where the tissue is rebuilt. Innate immune cells are major actors in the inflammatory response, of which, macrophages play an important role. Macrophages are highly sensitive to a large number of environmental stimuli, and can adapt their phenotype and function on demand. This change in phenotype in response to the environment allow macrophages to be involved in all steps of inflammation, from the first mounting of the pro-inflammatory response to the post-damage tissue repair.

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          Annexin A1 and glucocorticoids as effectors of the resolution of inflammation.

          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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            Cushing's syndrome.

            Cushing's syndrome results from lengthy and inappropriate exposure to excessive glucocorticoids. Untreated, it has significant morbidity and mortality. The syndrome remains a challenge to diagnose and manage. Here, we review the current understanding of pathogenesis, clinical features, diagnostic, and differential diagnostic approaches. We provide diagnostic algorithms and recommendations for management.
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              Neural regulation of innate immunity: a coordinated nonspecific host response to pathogens.

              The central nervous system (CNS) regulates innate immune responses through hormonal and neuronal routes. The neuroendocrine stress response and the sympathetic and parasympathetic nervous systems generally inhibit innate immune responses at systemic and regional levels, whereas the peripheral nervous system tends to amplify local innate immune responses. These systems work together to first activate and amplify local inflammatory responses that contain or eliminate invading pathogens, and subsequently to terminate inflammation and restore host homeostasis. Here, I review these regulatory mechanisms and discuss the evidence indicating that the CNS can be considered as integral to acute-phase inflammatory responses to pathogens as the innate immune system.
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                Author and article information

                Contributors
                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                09 July 2019
                2019
                : 10
                : 1591
                Affiliations
                [1] 1Institut NeuroMyoGène, Université Claude Bernard Lyon 1, Univ Lyon, CNRS UMR 5310, INSERM U1217 , Lyon, France
                [2] 2Institute of Comparative Molecular Endocrinology, University of Ulm , Ulm, Germany
                Author notes

                Edited by: Claude Libert, Flanders Institute for Biotechnology, Belgium

                Reviewed by: Inez Rogatsky, Hospital for Special Surgery, United States; Heinz Baumann, University at Buffalo, United States

                *Correspondence: Bénédicte Chazaud benedicte.chazaud@ 123456inserm.fr

                This article was submitted to Inflammation, a section of the journal Frontiers in Immunology

                †These authors have contributed equally to this work

                Article
                10.3389/fimmu.2019.01591
                6632423
                31354730
                9b135093-504c-4cdd-b8f2-dde2d373b178
                Copyright © 2019 Desgeorges, Caratti, Mounier, Tuckermann and Chazaud.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 16 April 2019
                : 25 June 2019
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 148, Pages: 12, Words: 10326
                Categories
                Immunology
                Mini Review

                Immunology
                glucocorticoids,macrophages,inflammation,tissue repair,phagocytosis glucocorticoid receptor

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