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      Inflammation in gastrointestinal disorders: prevalent socioeconomic factors

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          Abstract

          Western populations harbor a chronic inflammation pattern that lacks organ cardinal signs (edema, increased temperature, pain, and impaired function), releases increased levels of C-reactive protein, and often runs a creeping clinical course with generalized debilitating disease superimposed on system-specific involvement, mostly including nervous tissue (multiple sclerosis, Parkinson’s syndromes), joints (arthritis), and skin (psoriasis). A finalistic interpretation may apply to the consideration of the gut as the source of inflammation. In fact, these kind of local events as well as the remote manifestations named above, could be conditioned by the microbiome, the huge cell population indwelling the gut which is under growing scrutiny. The role of the gut as a barrier organ justifies lingering submucosal inflammation as a patrolling activity to maintain bodily integrity; the microbiome, launching inflammogenic signals in response to abrupt diet changes, confers to gut inflammation a socioeconomic vector calling for hitherto unrecognized multi-disciplinary interventions.

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          Most cited references49

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          The role of inflammation in depression: from evolutionary imperative to modern treatment target.

          Crosstalk between inflammatory pathways and neurocircuits in the brain can lead to behavioural responses, such as avoidance and alarm, that are likely to have provided early humans with an evolutionary advantage in their interactions with pathogens and predators. However, in modern times, such interactions between inflammation and the brain appear to drive the development of depression and may contribute to non-responsiveness to current antidepressant therapies. Recent data have elucidated the mechanisms by which the innate and adaptive immune systems interact with neurotransmitters and neurocircuits to influence the risk for depression. Here, we detail our current understanding of these pathways and discuss the therapeutic potential of targeting the immune system to treat depression.
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            Fecal Microbiota Transplantation Induces Remission in Patients With Active Ulcerative Colitis in a Randomized Controlled Trial.

            Ulcerative colitis (UC) is difficult to treat, and standard therapy does not always induce remission. Fecal microbiota transplantation (FMT) is an alternative approach that induced remission in small series of patients with active UC. We investigated its safety and efficacy in a placebo-controlled randomized trial.
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              Nod2 is a general sensor of peptidoglycan through muramyl dipeptide (MDP) detection.

              Nod2 activates the NF-kappaB pathway following intracellular stimulation by bacterial products. Recently, mutations in Nod2 have been shown to be associated with Crohn's disease, suggesting a role for bacteria-host interactions in the etiology of this disorder. We show here that Nod2 is a general sensor of peptidoglycan through the recognition of muramyl dipeptide (MDP), the minimal bioactive peptidoglycan motif common to all bacteria. Moreover, the 3020insC frameshift mutation, the most frequent Nod2 variant associated with Crohn's disease patients, fully abrogates Nod2-dependent detection of peptidoglycan and MDP. Together, these results impact on the understanding of Crohn's disease development. Additionally, the characterization of Nod2 as the first pathogen-recognition molecule that detects MDP will help to unravel the well known biological activities of this immunomodulatory compound.
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                Author and article information

                Journal
                Clin Exp Gastroenterol
                Clin Exp Gastroenterol
                CEG
                ceg
                Clinical and Experimental Gastroenterology
                Dove
                1178-7023
                19 July 2019
                2019
                : 12
                : 321-329
                Affiliations
                [1 ]Department of Surgical Sciences, University of Turin , Turin, Italy
                [2 ]Unit of Gastroenterology, Molinette-San Giovanni Antica Sede (SGAS) Hospital , Turin, Italy
                [3 ]The Medical Center Practice Office , Turin, Italy
                Author notes
                Correspondence: Davide Giuseppe RibaldoneDepartment of Surgical Sciences, University of Turin , C.so Bramante 88, 10126Turin, ItalyTel +39 011 633 3918Fax +39 011 633 3623Email davrib_1998@ 123456yahoo.com
                Author information
                http://orcid.org/0000-0002-9421-3087
                http://orcid.org/0000-0003-3438-0649
                http://orcid.org/0000-0001-7807-557X
                Article
                210844
                10.2147/CEG.S210844
                6650093
                d304fac6-3f9f-4c42-97ba-36596f80a71c
                © 2019 Ribaldone et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 01 April 2019
                : 24 June 2019
                Page count
                Figures: 1, Tables: 1, References: 63, Pages: 9
                Categories
                Review

                Gastroenterology & Hepatology
                colorectal cancer,inflammation,inflammatory bowel disease,irritable bowel syndrome,microbiome

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