Research Highlights: The Teamwork of Neutrophil and Macrophage to Kill Bacterial Pathogens

Science Picture Co / Getty Images

The Teamwork of Neutrophil and Macrophage to Kill Bacterial Pathogens

  • Staphylococcus aureus is a common Gram-positive round-shaped bacterium that is a member of the Firmicutes.
  • S. aureus is usually part of the human body’s microbiome however, it causes a wide range of illnesses which includes skin infections, food poisoning, and bone/joint infections.[2]
  • S. aureus is the primary cause of bacterial endocarditis and the second most frequent agent of bloodstream infections.
  • Bacterial endocarditis is a bacterial infection of the inner layer of the heart.[3]
  • Immune cells such as neutrophils and macrophages are capable of combating bacterial pathogens.
  • Neutrophils and macrophages are important to the innate immune response.
  • However, cooperative mechanisms used by neutrophils and macrophages to combat extracellular pathogens are not well understood.
  • During infection, neutrophils engulf S. aureus and then initiates bacterial elimination by producing reactive oxygen species or fusing granules containing antimicrobial compounds to the engulfed bacteria.
  • Additionally, neutrophils fight extracellular pathogens by producing extracellular “nets” consisting of DNA that can bind and trap pathogens.
  • The production of extracellular “nets” by neutrophils is called netosis.
  • Researchers discovered that S100A9-deficient neutrophils produce high levels of mitochondrial superoxide in response to S. aureus resulting in the formation of extracellular “nets”.
  • Increased suicidal netosis does not improve neutrophil killing of S. aureus in isolation but improves macrophage killing.
  • The “net” formation improves antibacterial activity with better engulfment capabilities of macrophages and transferring neutrophil-specific antimicrobial compounds to them.
  • Researchers observed similar results in response to other bacterial pathogens such as Streptococcus pneumoniae and Pseudomonas aeruginosa.
  • The findings suggest that achieving maximum antibacterial activity through these “net” formations requires macrophages.
  • Accelerated and more robust suicidal netosis makes neutrophils proficient at increasing antibacterial activity, especially when A9 deficient.