Arginine regulates the mucoid phenotype of hypervirulent Klebsiella pneumoniae

Abstract Hypervirulent Klebsiella pneumoniae causes severe community-acquired infections, with its mucoid phenotype resulting from altered capsular polysaccharide chain length. While both environmental and genetic factors influence mucoidy, the cues regulating it remain unclear. Here, we show that c...

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Main Authors: Brooke E. Ryan, Caitlyn L. Holmes, Drew J. Stark, Grace E. Shepard, Emma G. Mills, Saroj Khadka, Daria Van Tyne, Michael A. Bachman, Laura A. Mike
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-61047-y
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author Brooke E. Ryan
Caitlyn L. Holmes
Drew J. Stark
Grace E. Shepard
Emma G. Mills
Saroj Khadka
Daria Van Tyne
Michael A. Bachman
Laura A. Mike
author_facet Brooke E. Ryan
Caitlyn L. Holmes
Drew J. Stark
Grace E. Shepard
Emma G. Mills
Saroj Khadka
Daria Van Tyne
Michael A. Bachman
Laura A. Mike
author_sort Brooke E. Ryan
collection DOAJ
description Abstract Hypervirulent Klebsiella pneumoniae causes severe community-acquired infections, with its mucoid phenotype resulting from altered capsular polysaccharide chain length. While both environmental and genetic factors influence mucoidy, the cues regulating it remain unclear. Here, we show that casamino acids enhance mucoidy without affecting total capsular polysaccharide levels. We show that arginine is both necessary and sufficient in stimulating mucoid expression, activating the rmpADC promoter and increasing rmpADC transcript levels. The arginine regulator, ArgR, is crucial in this process; deleting argR reduces mucoidy and increases capsule chain length diversity. ArgR directly regulates the rmpADC promoter by binding to the ARG box. Loss of argR in vitro increases macrophage association and reduces competitive fitness in lungs, suggesting that ArgR influences adherence and fitness in the lung. Arginine-dependent regulation of mucoidy is conserved in hypervirulent K. pneumoniae isolates, suggesting that this regulatory mechanism broadly controls bacterial cell surface adaptations.
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spelling doaj-art-db9b02a78d334ba98d583eeaf96124562025-08-20T03:37:37ZengNature PortfolioNature Communications2041-17232025-07-0116111810.1038/s41467-025-61047-yArginine regulates the mucoid phenotype of hypervirulent Klebsiella pneumoniaeBrooke E. Ryan0Caitlyn L. Holmes1Drew J. Stark2Grace E. Shepard3Emma G. Mills4Saroj Khadka5Daria Van Tyne6Michael A. Bachman7Laura A. Mike8Medical Microbiology and Immunology, University of ToledoDepartment of Pathology, University of Michigan Medical SchoolDepartment of Medicine, Division of Infectious Diseases, University of PittsburghDepartment of Medicine, Division of Infectious Diseases, University of PittsburghDepartment of Medicine, Division of Infectious Diseases, University of PittsburghDepartment of Medicine, Division of Infectious Diseases, University of PittsburghDepartment of Medicine, Division of Infectious Diseases, University of PittsburghDepartment of Pathology, University of Michigan Medical SchoolDepartment of Medicine, Division of Infectious Diseases, University of PittsburghAbstract Hypervirulent Klebsiella pneumoniae causes severe community-acquired infections, with its mucoid phenotype resulting from altered capsular polysaccharide chain length. While both environmental and genetic factors influence mucoidy, the cues regulating it remain unclear. Here, we show that casamino acids enhance mucoidy without affecting total capsular polysaccharide levels. We show that arginine is both necessary and sufficient in stimulating mucoid expression, activating the rmpADC promoter and increasing rmpADC transcript levels. The arginine regulator, ArgR, is crucial in this process; deleting argR reduces mucoidy and increases capsule chain length diversity. ArgR directly regulates the rmpADC promoter by binding to the ARG box. Loss of argR in vitro increases macrophage association and reduces competitive fitness in lungs, suggesting that ArgR influences adherence and fitness in the lung. Arginine-dependent regulation of mucoidy is conserved in hypervirulent K. pneumoniae isolates, suggesting that this regulatory mechanism broadly controls bacterial cell surface adaptations.https://doi.org/10.1038/s41467-025-61047-y
spellingShingle Brooke E. Ryan
Caitlyn L. Holmes
Drew J. Stark
Grace E. Shepard
Emma G. Mills
Saroj Khadka
Daria Van Tyne
Michael A. Bachman
Laura A. Mike
Arginine regulates the mucoid phenotype of hypervirulent Klebsiella pneumoniae
Nature Communications
title Arginine regulates the mucoid phenotype of hypervirulent Klebsiella pneumoniae
title_full Arginine regulates the mucoid phenotype of hypervirulent Klebsiella pneumoniae
title_fullStr Arginine regulates the mucoid phenotype of hypervirulent Klebsiella pneumoniae
title_full_unstemmed Arginine regulates the mucoid phenotype of hypervirulent Klebsiella pneumoniae
title_short Arginine regulates the mucoid phenotype of hypervirulent Klebsiella pneumoniae
title_sort arginine regulates the mucoid phenotype of hypervirulent klebsiella pneumoniae
url https://doi.org/10.1038/s41467-025-61047-y
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