Limited proteolysis of neutrophil granule proteins by the bacterial protease RgpB depletes neutrophil antimicrobial capacity.

Neutrophils are highly abundant in the gingival tissues where they play an essential role in immune homeostasis by preventing microbial invasion. Here, we show that the oral periodontal pathogen Porphyromonas gingivalis utilizes its cysteine proteases (gingipains) to disengage phagosomal antimicrobial capacity. Arginine gingipains are a sub-family of trypsin-like proteases produced by P.

Dying for a cause: The pathogenic manipulation of cell death and efferocytic pathways.

Cell death is a natural consequence of infection. However, although the induction of cell death was solely thought to benefit the pathogen, compelling data now show that the activation of cell death pathways serves as a nuanced antimicrobial strategy that couples pathogen elimination with the generation of inflammatory cytokines and the priming of innate and adaptive cellular immunity. Following cell death, the phagocytic uptake of the infected dead cell by antigen-presenting cells and the subsequent lysosomal fusion of the apoptotic body containing the pathogen serve as an important antimicrobial mechanism that furthers the development of downstream adaptive immune responses.

Altruistic death: Neutrophil apoptosis maintains gingival health.

Discussion on targeting LXR and PPAR agonists as therapeutic alternatives to ustekinumab therapy in LAD-1.