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You searched for subject:(Allograft microbiota). Showing records 1 – 2 of 2 total matches.

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University of Toronto

1. Prescod, Janice Evana. Optimized Analysis of the Lung Allograft Microbiota from Bronchoalveolar Lavage Fluid.

Degree: 2018, University of Toronto

Introduction: Use of bronchoalveolar lavage fluid (BALF) for analysis of the allograft microbiota in lung transplant recipients (LTR) by culture-independent analysis poses specific challenges due to its highly variable bacterial density. Approach: We developed a methodology to analyze low-density BALF using a serially diluted mock community and BALF from uninfected LTR. Methods/Results: A mock microbial community was used to establish the properties of true-positive taxa and contaminants in BALF. Contaminants had an inverse relationship with input bacterial density. Concentrating samples increased the bacterial density and the ratio of community taxa (signal) to contaminants (noise), whereas DNase treatment decreased density and signal:noise. Systematic removal of contaminants had an important impact on microbiota-inflammation correlations in BALF. Conclusions: There is an inverse relationship between microbial density and the proportion of contaminants within microbial communities across the density range of BALF. This study has implications for the analysis and interpretation of BALF microbiota.

M.Sc.

Advisors/Committee Members: Coburn, Bryan, Laboratory Medicine and Pathobiology.

Subjects/Keywords: Allograft microbiota; Bronchoalveolar Lavage Fluid; Lung Transplant; Microbiome; 0410

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Prescod, J. E. (2018). Optimized Analysis of the Lung Allograft Microbiota from Bronchoalveolar Lavage Fluid. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/91350

Chicago Manual of Style (16th Edition):

Prescod, Janice Evana. “Optimized Analysis of the Lung Allograft Microbiota from Bronchoalveolar Lavage Fluid.” 2018. Masters Thesis, University of Toronto. Accessed November 27, 2020. http://hdl.handle.net/1807/91350.

MLA Handbook (7th Edition):

Prescod, Janice Evana. “Optimized Analysis of the Lung Allograft Microbiota from Bronchoalveolar Lavage Fluid.” 2018. Web. 27 Nov 2020.

Vancouver:

Prescod JE. Optimized Analysis of the Lung Allograft Microbiota from Bronchoalveolar Lavage Fluid. [Internet] [Masters thesis]. University of Toronto; 2018. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/1807/91350.

Council of Science Editors:

Prescod JE. Optimized Analysis of the Lung Allograft Microbiota from Bronchoalveolar Lavage Fluid. [Masters Thesis]. University of Toronto; 2018. Available from: http://hdl.handle.net/1807/91350

2. Lamarthee, Baptiste. L'interleukine-22 dans la maladie du greffon contre l'hôte après allogreffe de cellules souches hématopoïétiques : Interleukine-22 in graft-versus-host disease after allogeneic stem cell transplantation.

Degree: Docteur es, Sciences de la vie et de la santé, 2014, Besançon

La maladie du greffon contre l’hôte (GVHD) reste la complication majeure de l’allogreffe de cellules soucheshématopoïétiques (allo-CSH). La GVHD résulte de l’activation de la réponse immunitaire et de la reconnaissanced’alloantigènes par les lymphocytes T (LT) du donneur, entrainant ainsi des lésions tissulaires principalement auniveau de la peau, des intestins et du foie. L’interleukine-22 (IL-22) est une cytokine sécrétée par les LT Th1,Th17 et les cellules de l’immunité innée (ILC). Compte tenu des propriétés de l’IL-22 dans les tissus cibles de laGVHD, nous avons évalué sa contribution dans la physiopathologie de la maladie à l’aide de modèlesexpérimentaux murins. Il apparaît que les souris qui reçoivent des lymphocytes T invalidés pour l’IL-22développent une maladie moins sévère, et leur mortalité est diminuée. L’IL-22 issue du greffon participe donc à lasévérité de la GVHD en favorisant l’inflammation systémique, mais aussi locale au niveau des organes cibles. Deplus, dans les intestins, l’IL-22 agit en synergie avec les interférons de type I pour amplifier l’inflammation de typeTh1 au cours de la GVHD. Chez l’homme, la GVHD est associée à une modification du microbiote intestinal.Nous avons montré que l’absence d’IL-22 semble favoriser la colonisation de lactobacilles au détriment declostridiums, ce qui pourrait également participer à la diminution de la GVHD intestinale. Enfin, nous avonsmontré que l’effet anti-tumoral est préservé malgré l’absence d’IL-22. Ces résultats permettent donc d’envisagerde nouvelles perspectives thérapeutiques dans le traitement de la GVHD.

Graft-versus-host disease (GVHD) is still the major complication after allogeneic stem cell transplantation. GVHDresults from the activation of the immune response and the recognition by donor T cells of alloantigens leading totissue injury, especially in skin, gut and liver. Interleukin-22 (IL-22) is a cytokine secreted by CD4+ T cells Th1 andTh17 but also by innate lymphoid cells (ILC). Given that IL-22 functions in the GVHD target tissues, weinvestigated its contribution in GVHD physiopathology using mouse experimental models. We showed that IL-22deficiency in donor cells reduced the severity of GVHD by limiting systemic and local inflammation. Moreover, inthe large intestine, IL-22 acts in synergy with type I interferon to increase Th1-like inflammation. In humans,GVHD severity is associated with microbiotal modification in the intestine. We demonstrated that IL-22 deficiencyin donor cells seems to favor lactobacillus colonization instead of clostridium. These changes of microbiotacomposition may reduce the severity of intestinal GVHD. Finally, we showed that the antitumor effect is preservedeven in absence of IL-22 donor cells. Overall, our data support the design of new clinical approaches aiming totarget IL-22 pathways in GVHD patients.

Advisors/Committee Members: Gaugler, Béatrice (thesis director).

Subjects/Keywords: Maladie du greffon contre l'hôte; Inflammation; Interleukine-22; Allogreffe de cellules souches hématopoîétiques; Microbiote intestinal; Graft versus host disease; Inflammation; Interleukine-22; Allograft of haematopoietic stem cells; Intestinal Microbiota; QW 568

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Lamarthee, B. (2014). L'interleukine-22 dans la maladie du greffon contre l'hôte après allogreffe de cellules souches hématopoïétiques : Interleukine-22 in graft-versus-host disease after allogeneic stem cell transplantation. (Doctoral Dissertation). Besançon. Retrieved from http://www.theses.fr/2014BESA3006

Chicago Manual of Style (16th Edition):

Lamarthee, Baptiste. “L'interleukine-22 dans la maladie du greffon contre l'hôte après allogreffe de cellules souches hématopoïétiques : Interleukine-22 in graft-versus-host disease after allogeneic stem cell transplantation.” 2014. Doctoral Dissertation, Besançon. Accessed November 27, 2020. http://www.theses.fr/2014BESA3006.

MLA Handbook (7th Edition):

Lamarthee, Baptiste. “L'interleukine-22 dans la maladie du greffon contre l'hôte après allogreffe de cellules souches hématopoïétiques : Interleukine-22 in graft-versus-host disease after allogeneic stem cell transplantation.” 2014. Web. 27 Nov 2020.

Vancouver:

Lamarthee B. L'interleukine-22 dans la maladie du greffon contre l'hôte après allogreffe de cellules souches hématopoïétiques : Interleukine-22 in graft-versus-host disease after allogeneic stem cell transplantation. [Internet] [Doctoral dissertation]. Besançon; 2014. [cited 2020 Nov 27]. Available from: http://www.theses.fr/2014BESA3006.

Council of Science Editors:

Lamarthee B. L'interleukine-22 dans la maladie du greffon contre l'hôte après allogreffe de cellules souches hématopoïétiques : Interleukine-22 in graft-versus-host disease after allogeneic stem cell transplantation. [Doctoral Dissertation]. Besançon; 2014. Available from: http://www.theses.fr/2014BESA3006

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