Neutrophil Activation Decreases Ability to Kill Oral Streptococcus gordonii

As first responders, neutrophils are a vital component of the host defense against oral pathogens, and their function is critical in preventing the progression of periodontal diseases. Streptococcus gordonii, a generally commensal oral bacterium, has been implicated in the pathogenesis of diseases by operating as a pathobiont with Porphyromonas gingivalis in periodontitis, and as an independent pathogen in infective endocarditis. Although the pathogenicity of S. gordonii is variable, its role in modulating, as well as responding to, host neutrophils remain, poorly understood. This study focuses on neutrophil activation, migration, and bactericidal activity towards S. gordonii. Our results found S. gordonii induced significant upregulation of surface markers CD63 and CD66 on neutrophils, a phenotypic change reminiscent of an oral neutrophil, and was enhanced by pre-activation of neutrophils by lipopolysaccharide (LPS) or the oral pathogen P. gingivalis. Co-incubations with P. gingivalis also led to a decreased ability of neutrophils to kill the normally commensal S. gordonii, though not other commensals with opportunistic pathogen potential, including Escherichia coli or Staphylococcus aureus. This increase in survival correlated with changes in phagosomal maturation, a decrease in cytoplasmic and phagosomal-associated granules, and increased IL-1β production. These results suggest oral streptococci may significantly contribute to oral neutrophil phenotypes associated with health, but introduction of oral pathogens can exacerbate a neutrophil shift and contribute to the persistence of S. gordonii, and its ability to contribute to the pathogenesis of periodontal disease.