Neutrophils modulate natural killer-mediated osteoclastogenesis during Aggregatibacter actinomycetemcomitans (JP2 clone) infection

The study investigates the interplay of neutrophils and natural-killer cells (NK) in mediating osseoresorption during infection of molar-incisor-pattern-periodontitis (MIPP). Human neutrophils from periodontally healthy and MIPP patients were inoculated with the periopathogen Aggregatibacter-actinomycetemcomitans (JP2) and their supernatants were exposed to NK to study their function and osteoclastogenesis promotion. A mouse MIPP model was used to compare disease progression following NK versus neutrophils depletion. The exposure of primary NK to supernatants of neutrophils inoculated with JP2 led to NK cell arrest and activation with enhanced osteoprotegerin expression. Incubation of monocytes with NK led to osteoclastogenesis, whereas NK that were pre-exposed to healthy neutrophil supernatant showed reduced osteoclastogenesis. In mice, NK depletion led to the similar bone phenotype as the neutrophil's depletion highlighting their role on osseoprotection. The present study portrays a key crosstalk between neutrophils and NK cells during JP2 infection as a central mechanism that regulates bone loss.

Automated summary

The study investigates the interaction between neutrophils and natural killer (NK) cells in mediating bone resorption during molar-incisor-pattern-periodontitis (MIPP) infection. Human neutrophils from healthy individuals and MIPP patients were infected with the periodontal pathogen Aggregatibacter-actinomycetemcomitans (JP2), and their supernatants were exposed to NK cells to examine their function and promotion of osteoclastogenesis. Depletion of NK cells in a mouse MIPP model showed similar bone phenotypes as neutrophil depletion, highlighting the role of their crosstalk in bone protection.