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      TSPO PET Imaging: From Microglial Activation to Peripheral Sterile Inflammatory Diseases?

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          Abstract

          Peripheral sterile inflammatory diseases (PSIDs) are a heterogeneous group of disorders that gathers several chronic insults involving the cardiovascular, respiratory, gastrointestinal, or musculoskeletal system and wherein inflammation is the cornerstone of the pathophysiology. In PSID, timely characterization and localization of inflammatory foci are crucial for an adequate care for patients. In brain diseases, in vivo positron emission tomography (PET) exploration of inflammation has matured over the last 20 years, through the development of radiopharmaceuticals targeting the translocator protein-18 kDa (TSPO) as molecular biomarkers of activated microglia. Recently, TSPO has been introduced as a possible molecular target for PSIDs PET imaging, making this protein a potential biomarker to address disease heterogeneity, to assist in patient stratification, and to contribute to predicting treatment response. In this review, we summarized the major research advances recently made in the field of TSPO PET imaging in PSIDs. Promising preliminary results have been reported in bowel, cardiovascular, and rheumatic inflammatory diseases, consolidated by preclinical studies. Limitations of TSPO PET imaging in PSIDs, regarding both its large expression in healthy peripheral tissues, unlike in central nervous system, and the production of peripheral radiolabeled metabolites, are also discussed, regarding their possible consequences on TSPO PET signal's quantification.

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          Abundant data link hypercholesterolaemia to atherogenesis. However, only recently have we appreciated that inflammatory mechanisms couple dyslipidaemia to atheroma formation. Leukocyte recruitment and expression of pro-inflammatory cytokines characterize early atherogenesis, and malfunction of inflammatory mediators mutes atheroma formation in mice. Moreover, inflammatory pathways promote thrombosis, a late and dreaded complication of atherosclerosis responsible for myocardial infarctions and most strokes. The new appreciation of the role of inflammation in atherosclerosis provides a mechanistic framework for understanding the clinical benefits of lipid-lowering therapies. Identifying the triggers for inflammation and unravelling the details of inflammatory pathways may eventually furnish new therapeutic targets.
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            Molecular Mechanisms That Influence the Macrophage M1–M2 Polarization Balance

            As an essential component of innate immunity, macrophages have multiple functions in both inhibiting or promoting cell proliferation and tissue repair. Diversity and plasticity are hallmarks of macrophages. Classical M1 and alternative M2 activation of macrophages, mirroring the Th1–Th2 polarization of T cells, represent two extremes of a dynamic changing state of macrophage activation. M1-type macrophages release cytokines that inhibit the proliferation of surrounding cells and damage contiguous tissue, and M2-type macrophages release cytokines that promote the proliferation of contiguous cells and tissue repair. M1–M2 polarization of macrophage is a tightly controlled process entailing a set of signaling pathways, transcriptional and posttranscriptional regulatory networks. An imbalance of macrophage M1–M2 polarization is often associated with various diseases or inflammatory conditions. Therefore, identification of the molecules associated with the dynamic changes of macrophage polarization and understanding their interactions is crucial for elucidating the molecular basis of disease progression and designing novel macrophage-mediated therapeutic strategies.
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              The immunology of atherosclerosis

              Chronic kidney disease accelerates atherosclerosis via augmentation of inflammation, perturbation of lipid metabolism, and other mechanisms. Here, the authors describe the role of the immune system in the initiation and progression of atherosclerosis and discuss potential opportunities for therapy.
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                Author and article information

                Contributors
                Journal
                Contrast Media Mol Imaging
                Contrast Media Mol Imaging
                CMMI
                Contrast Media & Molecular Imaging
                Hindawi
                1555-4309
                1555-4317
                2017
                25 September 2017
                : 2017
                : 6592139
                Affiliations
                1CHRU Tours, 2 Boulevard Tonnellé, 37044 Tours, France
                2Institut National de la Santé et de la Recherche Médicale U930, 10 Boulevard Tonnellé, 37032 Tours, France
                Author notes

                Academic Editor: Anne Roivainen

                Author information
                http://orcid.org/0000-0002-6824-7283
                http://orcid.org/0000-0002-5095-9805
                Article
                10.1155/2017/6592139
                5632884
                29114179
                61085f36-4aa0-4339-bf45-c387f4f5ffec
                Copyright © 2017 Bérenger Largeau 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
                : 26 May 2017
                : 1 August 2017
                : 7 August 2017
                Funding
                Funded by: French National Agency for Research
                Award ID: ANR-11-LABX-0018-01
                Funded by: IRON
                Funded by: Seventh Framework Programme
                Award ID: 278850
                Categories
                Review Article

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