A surface protein identified from Streptococcus suis serotype 2 exhibits neutrophil-resistant ability via its...

Area of Science:

• Microbiology
• Immunology
• Zoonotic Diseases

Background:

• Streptococcus suis serotype 2 (SS2) is an emerging zoonotic pathogen causing various diseases.
• SS2 septicemia indicates evasion of innate immune cell defenses, but mechanisms are unclear.
• Neutrophils are crucial for innate immunity against bacterial infections.

Purpose of the Study:

• To investigate the mechanisms by which SS2 evades neutrophil-mediated immunity.
• To identify bacterial virulence factors involved in SS2 survival against innate immune cells.
• To explore potential targets for preventing and controlling swine streptococcosis.

Main Methods:

• Construction and characterization of a cell surface protein (CSP) deletion mutant (ΔCSP) of SS2.
• Assessment of neutrophil extracellular trap (NET) release and reactive oxygen species (ROS) formation.
• Evaluation of bacterial survival and proliferation within neutrophils and NETs.
• Analysis of extracellular signal-regulated kinase 1/2 (ERK1/2) signaling in neutrophils.

Main Results:

• The ΔCSP mutant showed a defective polysaccharide capsule and enhanced biofilm formation.
• ΔCSP induced increased NET release and ROS production compared to wild-type SS2.
• Bacterial survival and proliferation were significantly reduced in neutrophils and NETs for ΔCSP.
• Purified SS2 polysaccharide capsule inhibited neutrophil bactericidal activity.
• ΔCSP stimulated ERK1/2 signaling in neutrophils, potentially enhancing bacterial killing.

Conclusions:

• The SS2 polysaccharide capsule is a key virulence factor that inhibits neutrophil clearance.
• The cell surface protein (CSP) plays a role in SS2 evasion of innate immunity.
• Targeting the SS2 capsule or CSP could be a strategy for controlling swine streptococcosis.