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Brain-gut-microbiota axis in Parkinson's disease

World Journal of Gastroenterology 2015年第37期21卷 10609-10620页

作者： Agata Mulak bruno bonaz Department of Gastroenterology and Hepatology Wroclaw Medical University Grenoble Institut des Neurosciences (GIN) INSERM U836 38043 Grenoble France Clinique Universitaire d’Hépato-Gastroentérologie CHU de Grenoble 38043 Grenoble France

Parkinson's disease(PD) is characterized by alphasynucleinopathy that affects all levels of the braingut axis including the central, autonomic, and enteric nervous systems. Recently, it has been recognized that the brain-gut axis interactions are significantly modulated by the gut microbiota via immunological,neuroendocrine, and direct neural mechanisms. Dysregulation of the brain-gut-microbiota axis in PD may be associated with gastrointestinal manifestations frequently preceding motor symptoms, as well as with the pathogenesis of PD itself, supporting the hypothesis that the pathological process is spread from the gut to the brain. Excessive stimulation of the innate immune system resulting from gut dysbiosis and/or small intestinal bacterial overgrowth and increased intestinal permeability may induce systemic inflammation, while activation of enteric neurons and enteric glial cells may contribute to the initiation of alpha-synuclein ***, the adaptive immune system may be disturbed by bacterial proteins cross-reacting with human antigens. A better understanding of the brain-gutmicrobiota axis interactions should bring a new insight in the pathophysiology of PD and permit an earlier diagnosis with a focus on peripheral biomarkers within the enteric nervous system. Novel therapeutic options aimed at modifying the gut microbiota composition and enhancing the intestinal epithelial barrier integrity in PD patients could influence the initial step of the following cascade of neurodegeneration in PD.

关键词： Brain-gut-microbiota axis Enteric nervous system G

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Involvement of CRF2 signaling in enterocyte differentiation

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World Journal of Gastroenterology 2017年第28期23卷 5127-5145页

作者： Benjamin Ducarouge Marjolaine Pelissier-Rota Rebecca Powell Alain Buisson bruno bonaz Muriel Jacquier-Sarlin Equipe de l’apoptose du cancer et du développementCentre Léon Bérard Equipes des"Neuro-pathologies et Dysfonctions synaptiques"et du"Stress et des interactions neurodigestives" UniversitéGrenoble Alpes Equipes des"Neuropathologies et dysfonctions synaptiques"et du"Stress et des interactions neurodigestives" Université Grenoble Alpes and Grenoble Institut des Neurosciences-Inserm U1216 Service d’hépato-gastroentérologie Centre Hospitalier Universitaire de Grenoble

To determine the role of corticotropin releasing factor receptor (CRF2) in epithelial permeability and enterocyte cell *** this purpose, we used rat Sprague Dawley and various colon carcinoma cell lines (SW620, HCT8R, HT-29 and Caco-2 cell lines). Expression of CRF2 protein was analyzed by fluorescent immunolabeling in normal rat colon and then by western blot in dissociated colonic epithelial cells and in the lysates of colon carcinoma cell lines or during the early differentiation of HT-29 cells (ten first days). To assess the impact of CRF2 signaling on colonic cell differentiation, HT-29 and Caco-2 cells were exposed to Urocortin 3 recombinant proteins (Ucn3, 100 nmol/L). In some experiments, cells were pre-exposed to the astressin 2b (A2b) a CRF2 antagonist in order to inhibit the action of Ucn3. Intestinal cell differentiation was first analyzed by functional assays: the trans-cellular permeability and the para-cellular permeability were determined by Dextran-FITC intake and measure of the transepithelial electrical resistance respectively. Morphological modifications associated to epithelial dysfunction were analyzed by confocal microscopy after fluorescent labeling of actin (phaloidin-TRITC) and intercellular adhesion proteins such as E-cadherin, p120ctn, occludin and ZO-1. The establishment of mature adherens junctions (AJ) was monitored by following the distribution of AJ proteins in lipid raft fractions, after separation of cell lysates on sucrose gradients. Finally, the mRNA and the protein expression levels of characteristic markers of intestinal epithelial cell (IEC) differentiation such as the transcriptional factor krüppel-like factor 4 (KLF4) or the dipeptidyl peptidase IV (DPPIV) were performed by RT-PCR and western blot respectively. The specific activities of DPPIV and alkaline phosphatase (AP) enzymes were determined by a colorimetric ***2 protein is preferentially expressed in undifferentiated epithelial cel

关键词： Urocortin3 Colon carcinoma cell lines Intercellular adhesion complexes Cell permeability Epithelial cell differentiation Corticotrophin releasing factor 2

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Role of Cholinergic Receptors in Colorectal Cancer: Potential Therapeutic Implications of Vagus Nerve Stimulation?

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Journal of Cancer Therapy 2013年第6期4卷 1116-1131页

作者： Marjolaine Pelissier-Rota Michèle Lainé Benjamin Ducarouge bruno bonaz Muriel Jacquier-Sarlin Centre de Recherche Inserm U836 Institute of Neurosciences Grenoble France

Inflammatory Bowel Disease (IBD) patients, such as Crohn’s disease or ulcerative colitis suffer from chronic and relapsing intestinal inflammation that favours the development of colitis associated cancer (CAC). This inflammation is initiated by aberrant activations of the innate immune responses associated to intestinal barrier defects. The conventional medical therapies consist to decrease the inflammatory response, which also decrease the risk of colon carcinoma but lead to severe side-effects. Recently, a number of animal studies have demonstrated that innate immune responses are attenuated by stimulation of the efferent arm of vagus nerve (VN) through its neurotransmitter acetylcholine (ACh), that acts on resident macrophages α7 nicotinic receptor (α7 nAChR). ACh also acts as a signalling molecule in epithetlial cells through cholinergic receptors such as nAChR or muscarinic (mAChR) receptors. In the current study, we aimed to extend these findings to CAC prevention by treating human adenocarcinoma cell lines through targeting cholinergic receptors with nicotine (which binds nAChR) and ACh (which binds both cholinergic receptors). Using HT-29 and Caco-2 cell lines, we demonstrated that ACh-induced activation of mAChR results in cell dissociation together with changes in expression and localization of intestinal tight and adherens junction proteins. ACh-induced modulation of cell adhesion proprieties correlates with the acquisition of invasive potential. By contrast, nicotine-mediated activation of nAChR maintains epithelial cell organisation. ACh-released by VN stimulation (VNS) could effectively preserve epithelium integrity thus limiting inflammatory response and tumor development. However, attention should be paid on the nature of the cholinergic receptor solicited. Indeed, regarding to the protective effects of nAChR signalling on epithelial cells, activation of mAChR would worsen the disease and led to increase inflammation. These data have important reper

关键词： Cell Adhesion Colorectal Cancer Tumor Progression Cholinergic Receptors Inflammation Vagus Nerve

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