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      Resolution of PMA-Induced Skin Inflammation Involves Interaction of IFN- γ and ALOX15

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          Abstract

          Background. Acute inflammation and its timely resolution play important roles in the body's responses to the environmental stimulation. Although IFN- γ is well known for the induction of inflammation, its role in the inflammation resolution is still poorly understood. Methodology and Principal Findings. In this study, we investigated the function of interferon gamma (IFN- γ) during the resolution of PMA-induced skin inflammation in vivo. The results revealed that the expression levels of IL-6, TNF- α, and monocyte chemoattractant protein 1 (MCP-1) in skin decreased during the resolution stage of PMA-induced inflammation, while IFN- γ is still maintained at a relatively high level. Neutralization of endogenous IFN- γ led to accelerated reduction of epidermal thickness and decreased epithelial cell proliferation. Similarly, decreased infiltration of inflammatory cells (Gr1 + or CD11b + cells) and a significant reduction of proinflammatory cytokines were also observed upon the blockade of IFN- γ. Furthermore, neutralization of IFN- γ boosted ALOX15 expression of the skin during inflammation resolution. In accordance, application of lipoxin A4 (LXA4, a product of ALOX15) obtained a proresolution effect similar to neutralization of IFN- γ. These results demonstrated that through upregulating ALOX15-LXA4 pathway, blockage of IFN- γ can promote the resolution of PMA-induced skin inflammation.

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          Most cited references35

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          Inflammation is a complex set of interactions among soluble factors and cells that can arise in any tissue in response to traumatic, infectious, post-ischaemic, toxic or autoimmune injury. The process normally leads to recovery from infection and to healing, However, if targeted destruction and assisted repair are not properly phased, inflammation can lead to persistent tissue damage by leukocytes, lymphocytes or collagen. Inflammation may be considered in terms of its checkpoints, where binary or higher-order signals drive each commitment to escalate, go signals trigger stop signals, and molecules responsible for mediating the inflammatory response also suppress it, depending on timing and context. The non-inflammatory state does not arise passively from an absence of inflammatory stimuli; rather, maintenance of health requires the positive actions of specific gene products to suppress reactions to potentially inflammatory stimuli that do not warrant a full response.
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            Resolving inflammation: dual anti-inflammatory and pro-resolution lipid mediators.

            Active resolution of acute inflammation is a previously unrecognized interface between innate and adaptive immunity. Once thought to be a passive process, the resolution of inflammation is now shown to involve active biochemical programmes that enable inflamed tissues to return to homeostasis. This Review presents new cellular and molecular mechanisms for the resolution of inflammation, revealing key roles for eicosanoids, such as lipoxins, and recently discovered families of endogenous chemical mediators, termed resolvins and protectins. These mediators have anti-inflammatory and pro-resolution properties, thereby protecting organs from collateral damage, stimulating the clearance of inflammatory debris and promoting mucosal antimicrobial defence.
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              Resolution of inflammation: state of the art, definitions and terms.

              A recent focus meeting on Controlling Acute Inflammation was held in London, April 27-28, 2006, organized by D.W. Gilroy and S.D. Brain for the British Pharmacology Society. We concluded at the meeting that a consensus report was needed that addresses the rapid progress in this emerging field and details how the specific study of resolution of acute inflammation provides leads for novel anti-inflammatory therapeutics, as well as defines the terms and key components of interest in the resolution process within tissues as appreciated today. The inflammatory response protects the body against infection and injury but can itself become dysregulated with deleterious consequences to the host. It is now evident that endogenous biochemical pathways activated during defense reactions can counter-regulate inflammation and promote resolution. Hence, resolution is an active rather than a passive process, as once believed, which now promises novel approaches for the treatment of inflammation-associated diseases based on endogenous agonists of resolution.
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                Author and article information

                Journal
                Mediators Inflamm
                Mediators Inflamm
                MI
                Mediators of Inflammation
                Hindawi Publishing Corporation
                0962-9351
                1466-1861
                2013
                2 June 2013
                : 2013
                : 930124
                Affiliations
                1Research Center for Immunology, Xinxiang Medical University, 601 Jinsui Road, Xinxiang, Henan 453003, China
                2Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Beijing 100101, China
                3Graduate School of the Chinese Academy of Sciences, No.19A Yuquan Road, Beijing 100049, China
                Author notes

                Academic Editor: Elena Voronov

                Author information
                https://orcid.org/0000-0001-9793-7964
                Article
                10.1155/2013/930124
                3683498
                23818745
                4be265a2-26e8-422d-8951-3fafdff1fe88
                Copyright © 2013 Guojun Zhang et al.

                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
                : 18 January 2013
                : 7 April 2013
                : 7 May 2013
                Funding
                Funded by: 501100001809 National Natural Science Foundation of China
                Award ID: 81030049
                Funded by: 501100001809 National Natural Science Foundation of China
                Award ID: 91229203
                Categories
                Research Article

                Immunology
                Immunology

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