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2 results on '"Hannah L McMichael"'

1. Microbiota of MR1 deficient mice confer resistance against Clostridium difficile infection.

Author

Ashley D Smith, Elissa D Foss, Irma Zhang, Jessica L Hastie, Nicole P Giordano, Lusine Gasparyan, Lam Phuc VinhNguyen, Alyxandria M Schubert, Deepika Prasad, Hannah L McMichael, Jinchun Sun, Richard D Beger, Vahan Simonyan, Siobhán C Cowley, and Paul E Carlson

Subjects
Medicine, Science
Abstract

Clostridium difficile (Cd) infection (CDI) typically occurs after antibiotic usage perturbs the gut microbiota. Mucosa-associated invariant T cells (MAIT) are found in the gut and their development is dependent on Major histocompatibility complex-related protein 1 (MR1) and the host microbiome. Here we were interested in determining whether the absence of MR1 impacts resistance to CDI. To this end, wild-type (WT) and MR1-/- mice were treated with antibiotics and then infected with Cd spores. Surprisingly, MR1-/- mice exhibited resistance to Cd colonization. 16S rRNA gene sequencing of feces revealed inherent differences in microbial composition. This colonization resistance was transferred from MR1-/- to WT mice via fecal microbiota transplantation, suggesting that MR1-dependent factors influence the microbiota, leading to CDI susceptibility.

Published
2019
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2. Microbiota of MR1 deficient mice confer resistance against Clostridium difficile infection

Author

Irma Zhang, Deepika Prasad, Siobhán C. Cowley, Alyxandria M. Schubert, Ashley D. Smith, Richard D. Beger, Jinchun Sun, Elissa D. Foss, Hannah L. McMichael, Nicole P. Giordano, Paul E. Carlson, Lam Phuc VinhNguyen, Vahan Simonyan, Jessica L. Hastie, and Lusine Gasparyan

Subjects
0301 basic medicine, Antibiotics, Gut flora, Database and Informatics Methods, Feces, Mice, Microbial Physiology, Medicine and Health Sciences, Colonization, Bacterial Physiology, Intestinal Mucosa, Disease Resistance, Mice, Knockout, Multidisciplinary, biology, Antimicrobials, Drugs, Genomics, Animal Models, Clostridium difficile, Fecal Microbiota Transplantation, Anti-Bacterial Agents, Specific Pathogen-Free Organisms, Experimental Organism Systems, Medical Microbiology, Medicine, Anatomy, Sequence Analysis, Research Article, medicine.drug_class, Clostridium Difficile, Bioinformatics, Science, Sequence Databases, Cefoperazone, Mouse Models, Colonisation resistance, Microbial Genomics, Research and Analysis Methods, Microbiology, Mucosal-Associated Invariant T Cells, Minor Histocompatibility Antigens, 03 medical and health sciences, Antibiotic resistance, Model Organisms, Microbial Control, medicine, Genetics, Animals, Humans, Microbiome, Bacterial Spores, Pharmacology, 030102 biochemistry & molecular biology, Bacteria, Gut Bacteria, Histocompatibility Antigens Class I, Organisms, Biology and Life Sciences, Bacteriology, biology.organism_classification, Gastrointestinal Microbiome, Gastrointestinal Tract, Disease Models, Animal, 030104 developmental biology, Biological Databases, Antibiotic Resistance, Animal Studies, Clostridium Infections, Antimicrobial Resistance, Digestive System
Abstract

Clostridium difficile (Cd) infection (CDI) typically occurs after antibiotic usage perturbs the gut microbiota. Mucosa-associated invariant T cells (MAIT) are found in the gut and their development is dependent on Major histocompatibility complex-related protein 1 (MR1) and the host microbiome. Here we were interested in determining whether the absence of MR1 impacts resistance to CDI. To this end, wild-type (WT) and MR1-/- mice were treated with antibiotics and then infected with Cd spores. Surprisingly, MR1-/- mice exhibited resistance to Cd colonization. 16S rRNA gene sequencing of feces revealed inherent differences in microbial composition. This colonization resistance was transferred from MR1-/- to WT mice via fecal microbiota transplantation, suggesting that MR1-dependent factors influence the microbiota, leading to CDI susceptibility.

Published
2019

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