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      Enteric Glia: A New Player in Abdominal Pain

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          Abstract

          Chronic abdominal pain is the most common gastrointestinal issue and contributes to the pathophysiology of functional bowel disorders and inflammatory bowel disease. Current theories suggest that neuronal plasticity and broad alterations along the brain-gut axis contribute to the development of chronic abdominal pain, but the specific mechanisms involved in chronic abdominal pain remain incompletely understood. Accumulating evidence implicates glial cells in the development and maintenance of chronic pain. Astrocytes and microglia in the central nervous system and satellite glia in dorsal root ganglia contribute to chronic pain states through reactive gliosis, the modification of glial networks, and the synthesis and release of neuromodulators. In addition, new data suggest that enteric glia, a unique type of peripheral glia found within the enteric nervous system, have the potential to modify visceral perception through interactions with neurons and immune cells. Understanding these emerging roles of enteric glia is important to fully understand the mechanisms that drive chronic pain and to identify novel therapeutic targets. In this review, we discuss enteric glial cell signaling mechanisms that have the potential to influence chronic abdominal pain.

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          Pain regulation by non-neuronal cells and inflammation

          Acute pain is protective and a cardinal feature of inflammation. Chronic pain after arthritis, nerve injury, cancer, and chemotherapy is associated with chronic neuroinflammation, a local inflammation in the peripheral or central nervous system. Accumulating evidence suggests that non-neuronal cells such as immune cells, glial cells, keratinocytes, cancer cells, and stem cells play active roles in the pathogenesis and resolution of pain. We review how non-neuronal cells interact with nociceptive neurons by secreting neuroactive signaling molecules that modulate pain. Recent studies also suggest that bacterial infections regulate pain through direct actions on sensory neurons, and specific receptors are present in nociceptors to detect danger signals from infections. We also discuss new therapeutic strategies to control neuroinflammation for the prevention and treatment of chronic pain.
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            Noxious cold ion channel TRPA1 is activated by pungent compounds and bradykinin.

            Six members of the mammalian transient receptor potential (TRP) ion channels respond to varied temperature thresholds. The natural compounds capsaicin and menthol activate noxious heat-sensitive TRPV1 and cold-sensitive TRPM8, respectively. The burning and cooling perception of capsaicin and menthol demonstrate that these ion channels mediate thermosensation. We show that, in addition to noxious cold, pungent natural compounds present in cinnamon oil, wintergreen oil, clove oil, mustard oil, and ginger all activate TRPA1 (ANKTM1). Bradykinin, an inflammatory peptide acting through its G protein-coupled receptor, also activates TRPA1. We further show that phospholipase C is an important signaling component for TRPA1 activation. Cinnamaldehyde, the most specific TRPA1 activator, excites a subset of sensory neurons highly enriched in cold-sensitive neurons and elicits nociceptive behavior in mice. Collectively, these data demonstrate that TRPA1 activation elicits a painful sensation and provide a potential molecular model for why noxious cold can paradoxically be perceived as burning pain.
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              Burden of Gastrointestinal, Liver, and Pancreatic Diseases in the United States.

              Gastrointestinal (GI), liver, and pancreatic diseases are a source of substantial morbidity, mortality, and cost in the United States. Quantification and statistical analyses of the burden of these diseases are important for researchers, clinicians, policy makers, and public health professionals. We gathered data from national databases to estimate the burden and cost of GI and liver disease in the United States.
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                Author and article information

                Contributors
                Journal
                Cell Mol Gastroenterol Hepatol
                Cell Mol Gastroenterol Hepatol
                Cellular and Molecular Gastroenterology and Hepatology
                Elsevier
                2352-345X
                2019
                24 November 2018
                : 7
                : 2
                : 433-445
                Affiliations
                [1]Neuroscience Program, Department of Physiology, Michigan State University, East Lansing, Michigan
                Author notes
                [] Correspondence Address correspondence to: Brian D. Gulbransen, PhD, Neuroscience Program and Department of Physiology, Michigan State University, 567 Wilson Road, East Lansing, Michigan 48824. fax: (517) 355-5125. gulbrans@ 123456msu.edu
                Article
                S2352-345X(18)30168-1
                10.1016/j.jcmgh.2018.11.005
                6369218
                30739868
                74165ef2-1528-46ef-a503-d164de64f921
                © 2019 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 4 September 2018
                : 19 November 2018
                Categories
                Review

                glial cells,enteric glia,ens,abdominal pain,chronic pain,inflammation,brain-gut axis,atp, adenosine triphosphate,bdnf, brain-derived neurotrophic factor,cx-43, connexin-43,drg, dorsal root ganglia,gfap, glial fibrillary acidic protein,gi, gastrointestinal,ibd, irritable bowel disease,ibs, irritable bowel syndrome,il, interleukin,tnf, tumor necrosis factor,trpv1, transient receptor potential vanilloid receptor type-1

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