학술논문

An opportunistic pathogen under stress: how Group B Streptococcus responds to cytotoxic reactive species and conditions of metal ion imbalance to survive.
Document Type
Academic Journal
Author
Goh KGK; School of Pharmacy and Medical Sciences, and Menzies Health Institute Queensland, Griffith University, Parklands Drive, Southport, Gold Coast Campus, QLD 4222, Australia.; Desai D; School of Pharmacy and Medical Sciences, and Menzies Health Institute Queensland, Griffith University, Parklands Drive, Southport, Gold Coast Campus, QLD 4222, Australia.; Thapa R; School of Pharmacy and Medical Sciences, and Menzies Health Institute Queensland, Griffith University, Parklands Drive, Southport, Gold Coast Campus, QLD 4222, Australia.; Prince D; School of Pharmacy and Medical Sciences, and Menzies Health Institute Queensland, Griffith University, Parklands Drive, Southport, Gold Coast Campus, QLD 4222, Australia.; Acharya D; School of Pharmacy and Medical Sciences, and Menzies Health Institute Queensland, Griffith University, Parklands Drive, Southport, Gold Coast Campus, QLD 4222, Australia.; Sullivan MJ; School of Pharmacy and Medical Sciences, and Menzies Health Institute Queensland, Griffith University, Parklands Drive, Southport, Gold Coast Campus, QLD 4222, Australia.; School of Biological Sciences, University of East Anglia, Norwich Research Park, Norwich, NR4 7TJ, United Kingdom.; Ulett GC; School of Pharmacy and Medical Sciences, and Menzies Health Institute Queensland, Griffith University, Parklands Drive, Southport, Gold Coast Campus, QLD 4222, Australia.
Source
Publisher: Oxford University Press Country of Publication: England NLM ID: 8902526 Publication Model: Print Cited Medium: Internet ISSN: 1574-6976 (Electronic) Linking ISSN: 01686445 NLM ISO Abbreviation: FEMS Microbiol Rev Subsets: MEDLINE
Subject
Language
English
Abstract
Group B Streptococcus (GBS; also known as Streptococcus agalactiae) is an opportunistic bacterial pathogen that causes sepsis, meningitis, pneumonia, and skin and soft tissue infections in neonates and healthy or immunocompromised adults. GBS is well-adapted to survive in humans due to a plethora of virulence mechanisms that afford responses to support bacterial survival in dynamic host environments. These mechanisms and responses include counteraction of cell death from exposure to excess metal ions that can cause mismetallation and cytotoxicity, and strategies to combat molecules such as reactive oxygen and nitrogen species that are generated as part of innate host defence. Cytotoxicity from reactive molecules can stem from damage to proteins, DNA, and membrane lipids, potentially leading to bacterial cell death inside phagocytic cells or within extracellular spaces within the host. Deciphering the ways in which GBS responds to the stress of cytotoxic reactive molecules within the host will benefit the development of novel therapeutic and preventative strategies to manage the burden of GBS disease. This review summarizes knowledge of GBS carriage in humans and the mechanisms used by the bacteria to circumvent killing by these important elements of host immune defence: oxidative stress, nitrosative stress, and stress from metal ion intoxication/mismetallation.
(© The Author(s) 2024. Published by Oxford University Press on behalf of FEMS.)