Owing to the excellent antibacterial and antiviral activity, silver nanoparticles have a widespread use in the food and pharmaceutical industries. With the increase in the production and use of the related products, the potential hazard of silver nanoparticles has aroused public attention. The main purpose of this study is to explore the toxicity of silver nanoparticles and induction of lung inflammation in vitro and in vivo. Here, we validated that small amounts of silver ions dissolved from silver nanoparticles caused the depolarization of plasma membrane, resulting in an overload of intracellular sodium and calcium, and eventually led to the cell necrosis. The blockers of calcium or sodium channels inversed the toxicity of silver ions. Then, we instilled silver nanoparticles or silver nitrate (50 μg per mouse) into the lungs of mice, and this induced pulmonary injury and mitochondrial content release, led to the recruitment of neutrophils to the lung tissue via p38 MAPK pathway. Altogether, these data show that released silver ions from nanoparticles induced cell necrosis through Na⁺ and Ca²⁺ influx and triggered pulmonary inflammation through elevating mitochondrial-related contents released from these necrotic cells.

由于具有优异的抗菌和抗病毒活性，银纳米粒子在食品和制药行业得到广泛应用。随着相关产品产量和使用量的增加，纳米银的潜在危害引起了公众的关注。本研究的主要目的是探索银纳米粒子的毒性和体外和体内肺部炎症的诱导作用。在这里，我们验证了从银纳米粒子中溶解的少量银离子导致质膜去极化，导致细胞内钠和钙超载，最终导致细胞坏死。钙或钠通道的阻滞剂逆转了银离子的毒性。然后，我们将银纳米颗粒或硝酸银（每只小鼠 50 μg）注入小鼠的肺部，这导致肺损伤和线粒体内容物释放，导致中性粒细胞通过 p38 MAPK 途径募集到肺组织。总之，这些数据表明纳米颗粒释放的银离子通过钠离子诱导细胞坏死⁺和 Ca ²⁺流入并通过提高这些坏死细胞释放的线粒体相关内容物引发肺部炎症。