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Transmissible Staphylococcus pseudintermedius thwarts neutrophil extracellular trap-driven containment to promote

Rita Haller1,2, Yiyang Cai1,2,3,4,5,6,7, Nicole de Buhr8,9

  • 1Research Group Pathogenesis of Bacterial Infections; TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover, Germany.

Emerging Microbes & Infections
|April 2, 2025
PubMed

Insights

Methicillin-resistant Staphylococcus pseudintermedius (MRSP) uses a nuclease (NucB) to evade immune cells like neutrophils. This mechanism aids MRSP survival and infection in hosts, including potential zoonotic transmission to humans.

Area of Science:

  • Microbiology
  • Immunology
  • Zoonotic Diseases

Background:

  • Methicillin-resistant Staphylococcus pseudintermedius (MRSP) is an emerging zoonotic pathogen causing infections in animals and humans.
  • The immune evasion strategies of S. pseudintermedius remain poorly understood, hindering effective treatment and prevention.

Purpose of the Study:

  • To investigate the virulence mechanisms employed by MRSP to overcome host immune defenses, particularly neutrophil responses.
  • To elucidate the role of specific enzymes in MRSP pathogenicity and survival during infection.

Main Methods:

  • Utilized multi-tech imaging and a mouse model of bloodstream infection to study MRSP-host interactions.
  • Analyzed the function of thermostable nuclease (NucB) in MRSP's interaction with neutrophils and neutrophil extracellular traps (NETs).
  • Examined genetically distinct human clinical isolates for nuclease activity and resistance to NETosis.

Main Results:

  • MRSP employs a thermostable nuclease, NucB, to counteract antimicrobial and immobilizing effects of NETs.
  • NucB facilitates intra-neutrophil survival after phagocytosis, contributing to MRSP pathogenesis and persistence.
  • Human MRSP isolates exhibit nuclease activity and resistance to NETosis-induced killing, suggesting a conserved virulence mechanism.

Conclusions:

  • MRSP utilizes NucB to overcome innate immune responses, specifically neutrophilic attacks and NET-mediated killing.
  • This immune evasion mechanism is crucial for MRSP pathogenesis, persistence, and potential zoonotic transmission.
  • Understanding this mechanism offers insights into combating MRSP infections in both animals and humans.
Keywords:
NETosisStaphylococcus pseudintermediusimmune evasionnucleasezoonosis

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