A potential impact of Helicobacter pylori-related galectin-3 in neurodegeneration. (February 2018)

• Record Type: Journal Article
• Authors: Boziki, Marina; Polyzos, Stergios A.; Deretzi, Georgia; Kazakos, Evangelos; Katsinelos, Panagiotis; Doulberis, Michael; Kotronis, Georgios; Giartza-Taxidou, Evaggelia; Laskaridis, Leonidas; Tzivras, Dimitri; Vardaka, Elisabeth; Kountouras, Constantinos; Grigoriadis, Nikolaos; Thomann, Robert; Kountouras, Jannis
• Is Part Of: Neurochemistry international. Volume 113(2017)
• Page Start: 137
• Page End: 151
• Publication Date: 2018-02
• Subjects: Helicobacter pylori -- Galectin-3 -- Neurodegeneration -- Alzheimer's disease -- Central nervous system -- Inflammation; AD Alzheimer's disease -- AHF argentine haemorrhagic fever -- AGS human gastric adenoma carcinoma cells -- ALS Amyotrophic Lateral Sclerosis -- AMD age-related macular degeneration -- ANS Autonomous Nervous System -- AP-1 activation protein-1 -- APP amyloid precursor protein -- BabA Blood group antigen binding adhesin -- BBB blood-brain barrier -- BCR B-cell receptor -- BOB blood ocular barrier -- CCK-8 cholecystokinin octapeptide -- CJD Creutzfeldt-Jakob disease -- CNS Central Nervous System -- CIS Clinically Isolated Syndrome -- CRD carbohydrate-recognition domain -- CVD cardiovascular disease -- DAMPs danger-associated molecular patterns -- EAE Experimental Autoimmune Encephalomyelitis -- Gag PAI Gag pathogenicity island -- Gal-3 Galectin-3 -- GALT gut-associated lymphoid tissue -- GIT gastrointestinal tract -- Hcy homocysteine -- HPA hypothalamic-pituitary-adrenal -- Hp Helicobacter pylori -- IBD inflammatory bowel disease -- IFN interferon -- IL interleukin -- IRr insulin receptor -- JAK-STAT Janus kinase-signal transducer and activator of transcription -- JUNV Junín virus -- KO knock-out -- LPS lipopolysaccharide -- MAPK mitogen-activated protein kinase -- MCI Mild Cognitive impairment -- MetS metabolic syndrome -- MMP-9 metalloproteinase-9 -- MS Multiple Sclerosis -- NAFLD nonalcoholic fatty liver disease -- NAP neutrophil activating protein -- NASH nonalchoholic steatohepatis -- NF-κB nuclear factor-κB -- NOD1 Nucleotide-binding oligomerization domain 1 -- NMO neuromyelitis optica -- PAMP pathogen-associated molecular patterns -- PD Parkinson's disease -- POAG primary open-angle glaucoma -- PRR pattern-recognition receptors -- RGC retinal ganglion cells -- ROS reactive oxygen species -- RRMS relapsing-remitting multiple sclerosis -- SPMS secondary progressive MS -- siglecs sialic-acid immunoglobulin-like lectins -- SP substance P -- SST somatostatin -- SVZ sub-ventricular zone -- TBI Traumatic Brain Injury -- Th-1 T-helper type 1 -- Th-2 T-helper type 2 -- TLR toll-like receptors -- TNF tumor necrosis factor -- Tr-1 T-regulatory T-cells type 1 -- VacA Hp vacuolating cytotoxin A -- VIP vasoactive intestinal polypeptide -- VNs vasoactive neuropeptides; Neurochemistry -- Periodicals; Neurochemistry -- Periodicals; Neurochimie -- Périodiques; Neurochemistry; Periodicals; 612.804205
• DOI: 10.1016/j.neuint.2017.12.003
• Languages: English
• ISSNs: 0197-0186

Abstract

Abstract: Neurodegeneration represents a component of the central nervous system (CNS) diseases pathogenesis, either as a disability primary source in the frame of prototype neurodegenerative disorders, or as a secondary effect, following inflammation, hypoxia or neurotoxicity. Galectins are members of the lectin superfamily, a group of endogenous glycan-binding proteins, able to interact with glycosylated receptors expressed by several immune cell types. Glycan-lectin interactions play critical roles in the living systems by involving and mediating a variety of biologically important normal and pathological processes, including cell-cell signaling shaping cell communication, proliferation and migration, immune responses and fertilization, host-pathogen interactions and diseases such as neurodegenerative disorders and tumors. This review focuses in the role of Galectin-3 in shaping responses of the immune system against microbial agents, and concretely, Helicobacter pylori (Hp), thereby potentiating effect of the microbe in areas distant from the ordinary site of colonization, like the CNS. We hereby postulate that gastrointestinal Hp alterations in terms of immune cell functional phenotype, cytokine and chemokine secretion, may trigger systemic responses, thereby conferring implications for remote processes susceptible in immunity disequilibrium, namely, the CNS inflammation and/or neurodegeneration. Graphical abstract: Highlights: Galectins interact with glycosylated receptors expressed by epithelial/immune cells. Hp antigens/epitopes serve as immunogens locally and systematically. Hp infection induces Gal-3 expression by gastric epithelium. Gal-3 & Hp infection may pleitropically contribute to neurodegenerative pathologies. Mechanisms include: BBB breakdown, macrophage defects, IL-8, toxic agents and MetS.