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Cellina et al. Neuroimmunol Neuroinflammation 2018;5:22            Neuroimmunology
               DOI: 10.20517/2347-8659.2018.15                              and Neuroinflammation




               Commentary                                                                    Open Access


               Commentary on interactions between neurotropic
               pathogens, neuroinflammatory pathways, and

               autophagic neural cell death


               Michaela Cellina, Marcello Orsi

               Radiology Department, ASST Fatebenefratelli Sacco, Milan 20121, Italy.
               Correspondence to: Dr. Michaela Cellina, Radiology Department, ASST Fatebenefratelli Sacco, Piazza Principessa Clotilde,
               Milan 20121, Italy. E-mail: michaela.cellina@asst-fbf-sacco.it
               How to cite this article: Cellina M, Orsi M. Commentary on interactions between neurotropic pathogens, neuroinflammatory
               pathways, and autophagic neural cell death. Neuroimmunol Neuroinflammation 2018;5:22.
               http://dx.doi.org/10.20517/2347-8659.2018.15
               Received: 30 Mar 2018    First Decision: 2 May 2018    Revised: 7 May 2018    Accepted: 7 May 2018    Published: 5 Jun 2018

               Science Editor: Athanassios P. Kyritsis    Copy Editor: Guang-Zhe Zhu    Production Editor: Cai-Hong Wang


               Autophagy is a fundamental regulatory cellular mechanism, which enables cells to survive after a checked
               clearance of damaged organelles and proteins and a recycle of necessary molecules like amino acids and
               fatty acids to maintain homeostasis . There are a lot of factors able to influence autophagy in the states of
                                              [1]
               health and disease. In the excellent review by Sahu et al. , the role of autophagy, its mechanisms, and its
                                                                [2]
               protective role against the attack of pathogens are well described. However, even more controversial aspects
               of autophagy are addressed: first some pathogens, such as herpes simplex viruses, coxsackievirus, listeria
               monocytogenes have developed strategies to circumvent autophagy-dependent activation of host immune
               response, then some bacteria have the ability to modify the gene transcriptional level of the autophagic
               process, both in terms of downgrading of autophagy-related genes, as in the case of Yersinia enterocolitica
               and Francisella tularensis , and in terms of up regulation of autophagy-related genes: this mechanism favors
                                    [3]
               a prolonged inflammation at the infection site and results in further injury to surrounding healthy tissues,
               causing brain matter degeneration.

               The proposed hypothesis that prolonged infections of the central nervous system (CNS) by neurotropic
               pathogens, if associated with underlying conditions, might play a role in the pathogenesis of neurodegenerative
               diseases and the connections between autophagy dysregulation and neurodegeneration are subjects of great
               interest in literature.


               Recent studies have demonstrated an intrinsic connection between selective autophagy impairment and
               neurodegenerative diseases, including Alzheimer’s disease (AD) , Parkinson’s disease (PD) [8-10] , Huntington’s
                                                                    [4-7]
                           © The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
                and indicate if changes were made.


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