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Sahu et al. Neuroimmunol Neuroinflammation 2018;5:2                Neuroimmunology
               DOI: 10.20517/2347-8659.2017.43                              and Neuroinflammation




               Review                                                                        Open Access


               Interactions between neurotropic pathogens,
               neuroinflammatory pathways, and autophagic neural

               cell death


               Priyadarshi Soumyaranjan Sahu , Eunice Ter 1,2
                                           1
               1 School of Medicine, International Medical University, Bukit Jalil, 57000 Kuala Lumpur, Malaysia.
               2 University of Edinburgh Medical School, 47/49 Little France Crescent, Edinburgh, EH16 4SB/EH16 4TJ, United Kingdom.

               Correspondence to: Dr. Priyadarshi Soumyaranjan Sahu, Division of Pathology, School of Medicine, International Medical
               University, Bukit Jalil, 57000 Kuala Lumpur, Malaysia. E-mail: priyadarshi_sahu@yahoo.com

               How to cite this article: Sahu PS, Ter E. Interactions between neurotropic pathogens, neuroinflammatory pathways, and autophagic
               neural cell death. Neuroimmunol Neuroinflammation 2018;5:2. http://dx.doi.org/10.20517/2347-8659.2017.43
               Received: 21 Aug 2017    First Decision: 23 Aug 2017    Revised: 30 Nov 2017    Accepted: 18 Dec 2017    Published: 17 Jan 2018

               Science Editor: Athanassios P. Kyritsis    Copy Editor: Lu Liu    Production Editor: Cai-Hong Wang


               Abstract

               In recent times, there has been a significant increase in studies focusing on immunological functions of autophagy,
               however, knowledge of its roles and regulations in the central nervous system remains unclear. Present reviews
               highlight the molecular cross talk between host cell autophagy with inflammatory pathways in the context of
               neuro-infections. Intracellular pathogens might have an ability to manipulate the autophagy regulation process. An
               augmented autophagy and inflammation at the site of infection is traditionally considered host protective. Moreover,
               host cell autophagy might also facilitate pathogen survivability and multiplication in the brain environment.
               Consequently, an excessive autophagy and neuroinflammatory process do put surrounding healthy brain tissue
               at risk of pathogen invasion. The question arises, whether there are any known direct interactions of intracellular
               neurotropic pathogens with this degradative pathway that favour intracerebral pathogen survival and growth? It
               is worth exploring any such cooperation between pathogen factors and altered immune pathways that modulate
               autophagy regulatory genes causing massive neuronal damage. A detailed understanding of molecular mechanisms
               in microbial pathogenesis, neuroinflammatory and neuronal autophagy pathways might identify novel therapeutic
               targets and diagnostic biomarkers.

               Keywords: Central nervous system infection, neurotropic pathogens, neuroinflammation, autophagy


               INTRODUCTION
               Neurotropism of certain microbial pathogens could lead to neurological health problems in humans. It is
               suggested that chronic infections in the central nervous system (CNS) might be associated with progressive

                           © 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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