CFTR-PTEN–dependent mitochondrial metabolic dysfunction promotes Pseudomonas aeruginosa airway infection

Author:

Riquelme Sebastián A.1ORCID,Lozano Carmen2ORCID,Moustafa Ahmed M.3ORCID,Liimatta Kalle1ORCID,Tomlinson Kira L.1ORCID,Britto Clemente4ORCID,Khanal Sara4ORCID,Gill Simren K.1,Narechania Apurva5,Azcona-Gutiérrez Jose M.6ORCID,DiMango Emily7,Saénz Yolanda2ORCID,Planet Paul3ORCID,Prince Alice1ORCID

Affiliation:

1. Department of Pediatrics, Columbia University, New York, NY 10032, USA.

2. Area de Microbiología Molecular, Centro de Investigación Biomédica de la Rioja (CIBIR), Microbiología Molecular, Logroño, LG 26006, Spain.

3. Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania and Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.

4. Section of Pulmonary, Critical Care, and Sleep Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.

5. American Museum of Natural History, New York, NY 10024, USA.

6. Departamento de Diagnóstico Biomédico. Laboratorio de Microbiología, Hospital San Pedro, Logroño, LG 26006, Spain.

7. Department of Medicine, Columbia University, New York, NY 10032, USA.

Abstract

Excess succinate due to CFTR-PTEN dysfunction selects for Pseudomonas aeruginosa mutants adapted to the airway.

Funder

NIH Office of the Director

Cystic Fibrosis Foundation

Pediatric Infectious Diseases Society

Instituto de Salud Carlos III

NCATS-NIH

Clinical and Translational Science Awards (CTSA), Integrating Special Populations (ISP) Resource, Columbia University

Clinical Doris Duke Clinical Scientist Development Award

CFF Pilot Grant

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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