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Manuella Bouttier, Ph.D.Research Associate and Lab ManagerPreviously Postdoctoral fellow in the lab Department of Physiology Ěý Phone: (514) 398-8555 manuella.bouttier [at] mail.mcgill.ca (Email) |
Project Summary:Our goals are to understand the host macrophage response to Mycobacterium tuberculosis (M.tb.) infection through the use of cutting-edge genomics techniques, as mRNA and miRNA microarrays and ChIP sequencing. We also study the role of vitamin D in boosting the innate immune responses to M.tb. infection. TB has been resurgent recently, and represents the leading cause of death from a curable disease. M. tuberculosis (M.tb.) replicates within cell of the immune system called macrophages, ultimately inducing cell death. Macrophages are sites of vitamin D signaling, and there is growing evidence that vitamin D modulates macrophage responses to M.tb. Vitamin D was discovered as the curative agent of nutritional rickets, which arises from insufficient uptake of dietary calcium. However, it is now apparent that vitamin D functions throughout the body, in particular in the immune system. Elevated levels of TB, have been associated with vitamin D deficiency, suggesting that vitamin D supplementation may be of therapeutic benefit. This multidisciplinary project combines metaregulation analysis, host-pathogen interactions and immunity. French VersionLa Tuberculose (TB) est une des causes majeures de mortalitĂ©, avec environ 2 milliards de personnes infectĂ©es Ă travers le monde. Mycobacterium tuberculosis (Mtb), l’agent Ă©tiologique de TB rĂ©side dans les macrophages. Par ailleurs, dĂ©couverte comme une hormone rĂ©gulant le taux de calcium, la vitamine D a Ă©tĂ© mise en Ă©vidence dans notre laboratoire comme un rĂ©gulateur important de l’immunitĂ© innĂ©e chez l’homme. En outre, la dĂ©ficience en vitamine D dans les populations vulnĂ©rables et immigrantes est associĂ©e avec des taux Ă©levĂ©s d’infection par TB.ĚýL’objectif principal de notre projet est de dĂ©terminer les mĂ©canismes molĂ©culaires et cellulaires par lesquels l’infection et la vitamine D coopèrent pour stimuler l’immunitĂ© innĂ©e des macrophages masculins Ă l’infection par M.tb. Pour cela, nous utilisons de nombreuses mĂ©thodes gĂ©nomiques (puces Ă ADN, ARN, miRNA, sĂ©quençage par ChIP) et des outils bio-informatiques afin d’intĂ©grer nos donnĂ©es transcriptomiques Ă notre système biologique. Ěý Ěý |
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Babak Memari, Ph.D., Postdoctoral FellowFormer PhD Student Department of Physiology Ěý Phone: 514-398-8555 babak.memari [at] mail.mcgill.ca (Email) |
Project Summary:M.tb. infection of macrophages leads to multiple signal transduction events, which alter the function of numerous transcription factors controlling the host transcriptional response to infection. We have evidence that infection induces the expression and function of a transcription factor called the arylhydrocarbon receptor (AHR) as well as its heterodimeric partners. Other studies have provided evidence that AHR function regulates innate immune responses in other cells types. Our goals are to understand how AHR signaling in macrophages controls innate immunity to M.tb. infection. French VersionL’infection par M.tb conduit Ă une multitude de signaux de transduction, qui module la fonction de nombreux facteurs de transcription contrĂ´lant eux-mĂŞmes, la rĂ©ponse transcriptomique de l’hĂ´te. Nous avons mis en Ă©vidence que l’infection induit l’expression et l’activation d’un facteur de transcription, appelĂ© rĂ©cepteur arylhydrocarboneĚý (AHR), ainsi que de ses co-facteurs hĂ©tĂ©rodimeriques. D’autres Ă©tudes ont montrĂ© que la protĂ©ine AHR agit comme rĂ©gulateur de la rĂ©ponse immunitaire innĂ©e dans d’autres types cellulaires. Notre objectif est que comprendre comment la signalisation via AHR conduit au contrĂ´le de l’infection par M.tb. Ěý |
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Joseph Mangiapane, Mscgraduated in Jan 2017 Department of Physiology Ěý Phone : 514-398-8555 joseph.mangiapane [at] mail.mcgill.ca (Email) |
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