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Improvement of a mouse infection model to capture Pseudomonas aeruginosa chronic physiology in cystic fibrosis.
Duncan, Rebecca P; Moustafa, Dina A; Lewin, Gina R; Diggle, Frances L; Bomberger, Jennifer M; Whiteley, Marvin; Goldberg, Joanna B.
Afiliación
  • Duncan RP; Division of Pulmonary, Asthma, Cystic Fibrosis, and Sleep, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322.
  • Moustafa DA; Emory-Children's Cystic Fibrosis Center, Atlanta, GA 30322.
  • Lewin GR; Division of Pulmonary, Asthma, Cystic Fibrosis, and Sleep, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322.
  • Diggle FL; Emory-Children's Cystic Fibrosis Center, Atlanta, GA 30322.
  • Bomberger JM; Emory-Children's Cystic Fibrosis Center, Atlanta, GA 30322.
  • Whiteley M; School of Biological Sciences and Center for Microbial Dynamics and Infection, Georgia Institute of Technology, Atlanta, GA 30322.
  • Goldberg JB; Emory-Children's Cystic Fibrosis Center, Atlanta, GA 30322.
Proc Natl Acad Sci U S A ; 121(33): e2406234121, 2024 Aug 13.
Article en En | MEDLINE | ID: mdl-39102545
ABSTRACT
Laboratory models are central to microbiology research, advancing the understanding of bacterial physiology by mimicking natural environments, from soil to the human microbiome. When studying host-bacteria interactions, animal models enable investigators to examine bacterial dynamics associated with a host, and in the case of human infections, animal models are necessary to translate basic research into clinical treatments. Efforts toward improving animal infection models are typically based on reproducing host genotypes/phenotypes and disease manifestations, leaving a gap in how well the physiology of microbes reflects their behavior in a human host. Understanding bacterial physiology is vital because it dictates host response and bacterial interactions with antimicrobials. Thus, our goal was to develop an animal model that accurately recapitulates bacterial physiology in human infection. The system we chose to model was a chronic Pseudomonas aeruginosa respiratory infection in cystic fibrosis (CF). To accomplish this goal, we leveraged a framework that we recently developed to evaluate model accuracy by calculating the percentage of bacterial genes that are expressed similarly in a model to how they are expressed in their infection environment. We combined two complementary models of P. aeruginosa infection-an in vitro synthetic CF sputum model (SCFM2) and a mouse acute pneumonia model. This combined model captured the chronic physiology of P. aeruginosa in CF better than the standard mouse infection model, showing the power of a data-driven approach to refining animal models. In addition, the results of this work challenge the assumption that a chronic infection model requires long-term colonization.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Pseudomonas aeruginosa / Infecciones por Pseudomonas / Fibrosis Quística / Modelos Animales de Enfermedad Límite: Animals / Humans Idioma: En Revista: Proc Natl Acad Sci U S A Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Pseudomonas aeruginosa / Infecciones por Pseudomonas / Fibrosis Quística / Modelos Animales de Enfermedad Límite: Animals / Humans Idioma: En Revista: Proc Natl Acad Sci U S A Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos