Restoring glucose uptake rescues neutrophil dysfunction and protects against systemic fungal infection in mouse models of kidney disease

Author:

Jawale Chetan V.1ORCID,Ramani Kritika1,Li De-dong1ORCID,Coleman Bianca M.1ORCID,Oberoi Rohan S.1ORCID,Kupul Saran1ORCID,Lin Li1,Desai Jigar V.2ORCID,Delgoffe Greg M.3,Lionakis Michail S.2,Bender Filitsa H.4,Prokopienko Alexander J.5ORCID,Nolin Thomas D.45ORCID,Gaffen Sarah L.1ORCID,Biswas Partha S.1ORCID

Affiliation:

1. Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15261, USA.

2. Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20814, USA.

3. Department of Immunology, University of Pittsburgh, Pittsburgh, PA 15261, USA.

4. Division of Renal-Electrolyte, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15261, USA.

5. Department of Pharmacy and Therapeutics, University of Pittsburgh, Pittsburgh, PA 15261, USA.

Abstract

Metabolic reprogramming with a GSK3β inhibitor corrects neutrophil dysfunction and improves antifungal function in mouse models of kidney disease.

Funder

National Institute of Allergy and Infectious Diseases

National Institute of Diabetes and Digestive and Kidney Diseases

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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