Human β-defensin 2 enhances IL-1β production and pyroptosis through P2X7-mediated NLRP3 expression in macrophages

Periodontal disease is the leading cause of tooth loss, which also a high-risk factor for other diseases including oral cancer and cardiovascular disease. Periodontitis one most common type periodontal diseases. Interleukin-1β (IL-1β) plays key role in pathogenesis periodontitis. However, mechanism how IL-1β produced during periodontitis still unclear. In present study, we found that human β-defensin 2 (hBD2) enhances production through an LPS-primed acute monocytic leukemia (THP-1) macrophage model. Inhibition P2X purinoceptor 7 (P2X7) reduced hBD2-enhanced production. Incubation THP-1 macrophages with potassium chloride suppressed Silence inflammasome adaptor Nod-like receptor family pyrin domain containing 3 (NLRP3) led to Likewise, inhibition caspase-1 resulted decrease IL-1β. Moreover, ethidium bromide uptake test indicated hBD2-activated mediated pyroptotic pore formation. Subsequent lactate dehydrogenase detection flow cytometric analysis hBD2 induced pyroptosis. brief, these findings illustrated not only enhancing inflammatory response, but provided novel therapeutic targets