An opportunistic pathogen under stress: How Group B Streptococcus responds to cytotoxic reactive species and conditions of metal ion imbalance to survive

Kelvin G. K. Goh, Devika Desai, Ruby Thapa, Darren Prince, Dhruba Acharya, Matthew J. Sullivan, Glen C. Ulett

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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.

Original languageEnglish
Article numberfuae009
JournalFEMS Microbiology Reviews
Volume48
Issue number3
Early online date27 Apr 2024
DOIs
Publication statusPublished - May 2024

Keywords

  • bacteria
  • copper
  • host-pathogen interactions
  • metal homeostasis
  • metal stress
  • metallobiology
  • pathogenesis
  • reactive nitrogen species
  • reactive oxygen species
  • zinc

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