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      Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines

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          Abstract

          Cytokine dysregulation is believed to play a key role in the remodeling of the immune system at older age, with evidence pointing to an inability to fine-control systemic inflammation, which seems to be a marker of unsuccessful aging. This reshaping of cytokine expression pattern, with a progressive tendency toward a pro-inflammatory phenotype has been called “inflamm-aging.” Despite research there is no clear understanding about the causes of “inflamm-aging” that underpin most major age-related diseases, including atherosclerosis, diabetes, Alzheimer’s disease, rheumatoid arthritis, cancer, and aging itself. While inflammation is part of the normal repair response for healing, and essential in keeping us safe from bacterial and viral infections and noxious environmental agents, not all inflammation is good. When inflammation becomes prolonged and persists, it can become damaging and destructive. Several common molecular pathways have been identified that are associated with both aging and low-grade inflammation. The age-related change in redox balance, the increase in age-related senescent cells, the senescence-associated secretory phenotype (SASP) and the decline in effective autophagy that can trigger the inflammasome, suggest that it may be possible to delay age-related diseases and aging itself by suppressing pro-inflammatory molecular mechanisms or improving the timely resolution of inflammation. Conversely there may be learning from molecular or genetic pathways from long-lived cohorts who exemplify good quality aging. Here, we will discuss some of the current ideas and highlight molecular pathways that appear to contribute to the immune imbalance and the cytokine dysregulation, which is associated with “inflammageing” or parainflammation. Evidence of these findings will be drawn from research in cardiovascular disease, cancer, neurological inflammation and rheumatoid arthritis.

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          Most cited references 457

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          Inflammation and cancer.

          Recent data have expanded the concept that inflammation is a critical component of tumour progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration. In addition, tumour cells have co-opted some of the signalling molecules of the innate immune system, such as selectins, chemokines and their receptors for invasion, migration and metastasis. These insights are fostering new anti-inflammatory therapeutic approaches to cancer development.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Immunity, inflammation, and cancer.

            Inflammatory responses play decisive roles at different stages of tumor development, including initiation, promotion, malignant conversion, invasion, and metastasis. Inflammation also affects immune surveillance and responses to therapy. Immune cells that infiltrate tumors engage in an extensive and dynamic crosstalk with cancer cells, and some of the molecular events that mediate this dialog have been revealed. This review outlines the principal mechanisms that govern the effects of inflammation and immunity on tumor development and discusses attractive new targets for cancer therapy and prevention. 2010 Elsevier Inc. All rights reserved.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Autophagy fights disease through cellular self-digestion.

              Autophagy, or cellular self-digestion, is a cellular pathway involved in protein and organelle degradation, with an astonishing number of connections to human disease and physiology. For example, autophagic dysfunction is associated with cancer, neurodegeneration, microbial infection and ageing. Paradoxically, although autophagy is primarily a protective process for the cell, it can also play a role in cell death. Understanding autophagy may ultimately allow scientists and clinicians to harness this process for the purpose of improving human health.
                Bookmark

                Author and article information

                Contributors
                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                09 April 2018
                2018
                : 9
                Affiliations
                1School of Medicine, Dentistry and Biomedical Science, Queens University Belfast , Belfast, United Kingdom
                2Northern Ireland Centre for Stratified Medicine, Biomedical Sciences Research Institute, University of Ulster, C-TRIC Building, Altnagelvin Area Hospital , Londonderry, United Kingdom
                3Care of Elderly Medicine, Belfast Health and Social Care Trust , Belfast, United Kingdom
                4Regional Genetics Service, Belfast Health and Social Care Trust , Belfast, United Kingdom
                5Department of Neuroscience, Mayo Clinic , Jacksonville, FL, United States
                6Department of Clinical Genomics, Mayo Clinic , Jacksonville, FL, United States
                7School of Medicine and Medical Science, University College Dublin , Dublin, Ireland
                Author notes

                Edited by: Rafael Solana, Universidad de Córdoba, Spain

                Reviewed by: Armando Luna López, Instituto Nacional de Geriatría, Mexico; Valerio Chiurchiù, Università Campus Bio-Medico, Italy; Beatriz Sánchez Correa, Universidad de Extremadura, Spain

                *Correspondence: Irene Maeve Rea, i.rea@ 123456qub.ac.uk

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

                Article
                10.3389/fimmu.2018.00586
                5900450
                Copyright © 2018 Rea, Gibson, McGilligan, McNerlan, Alexander and Ross.

                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 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.

                Page count
                Figures: 5, Tables: 0, Equations: 0, References: 459, Pages: 28, Words: 25394
                Categories
                Immunology
                Review

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