Proinflammatory responses triggerd by ricin toxin require macrophages and IL-1β signaling through the NALP3 inflammasome

Ricin is a ribotoxic stressor that blocks protein synthesis and activates stress‑activated protein kinases, but its mechanisms of inducing inflammation remain unclear. Because aerosolized ricin poses a significant bioterrorism risk, understanding its pulmonary effects is critical. This dissertation investigates ricin‑triggered inflammatory responses in the lungs of mice. The findings show that ricin exposure induces strong expression of inflammatory genes, edema, increased microvascular permeability, and pronounced neutrophil infiltration. These results identify key features of ricin‑mediated lung injury and help clarify the molecular basis of ricin‑induced inflammation.