The oxidative stress response of Streptococcus pneumoniae: its contribution to both extracellular and intracellular survival

Streptococcus pneumoniae is a gram-positive, aerotolerant bacterium that naturally colonizes the human nasopharynx, but also causes invasive infections and is a major cause of morbidity and mortality worldwide. This pathogen produces high levels of H 2 O 2 to eliminate other microorganisms that belo...

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Published in:Frontiers in microbiology Vol. 14; p. 1269843
Main Authors: Hernandez-Morfa, Mirelys, Olivero, Nadia B., Zappia, Victoria E., Piñas, German E., Reinoso-Vizcaino, Nicolas M., Cian, Melina B., Nuñez-Fernandez, Mariana, Cortes, Paulo R., Echenique, Jose
Format: Journal Article
Language:English
Published: Frontiers Media S.A 13-09-2023
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Summary:Streptococcus pneumoniae is a gram-positive, aerotolerant bacterium that naturally colonizes the human nasopharynx, but also causes invasive infections and is a major cause of morbidity and mortality worldwide. This pathogen produces high levels of H 2 O 2 to eliminate other microorganisms that belong to the microbiota of the respiratory tract. However, it also induces an oxidative stress response to survive under this stressful condition. Furthermore, this self-defense mechanism is advantageous in tolerating oxidative stress imposed by the host’s immune response. This review provides a comprehensive overview of the strategies employed by the pneumococcus to survive oxidative stress. These strategies encompass the utilization of H 2 O 2 scavengers and thioredoxins, the adaptive response to antimicrobial host oxidants, the regulation of manganese and iron homeostasis, and the intricate regulatory networks that control the stress response. Here, we have also summarized less explored aspects such as the involvement of reparation systems and polyamine metabolism. A particular emphasis is put on the role of the oxidative stress response during the transient intracellular life of Streptococcus pneumoniae , including coinfection with influenza A and the induction of antibiotic persistence in host cells.
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Present addresses: German E. Piñas, State of Utah, Department of Health, Salt Lake City, UT, United States; Nicolas M. Reinoso-Vizcaino, Department of Molecular Genetics and Microbiology, Duke Center for Virology, Duke University School of Medicine, Durham, NC, United States; Melina B. Cian, Health Sciences Center, University of Oklahoma, Norman, OK, United States
These authors have contributed equally to this work and the order of these authors is arbitrary
Edited by: Haike Antelmann, Freie Universität Berlin, Germany
Reviewed by: Jan-Ulrik Dahl, Illinois State University, United States; Stephanie Neville, The University of Melbourne, Australia; Claudia Trappetti, University of Adelaide, Australia
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2023.1269843