Dietary zinc deficiency is a major risk factor for pneumonia. Acinetobacter baumannii is a leading cause of ventilator-associated pneumonia and a critical public health threat due to increasing rates of multidrug resistance. Patient populations at increased risk for A. baumannii pneumonia are also at increased risk of zinc deficiency. Here we established a mouse model of dietary zinc deficiency and acute A. baumannii pneumonia to test the hypothesis that host zinc deficiency contributes to A. baumannii pathogenesis. We showed that zinc-deficient mice have significantly increased A. baumannii burdens in the lungs, dissemination to the spleen and higher mortality. During infection, zinc-deficient mice produce more pro-inflammatory cytokines, including IL-13. Administration of IL-13 promotes A. baumannii dissemination in zinc-sufficient mice, while antibody neutralization of IL-13 protects zinc-deficient mice from A. baumannii dissemination and mortality during infection. These data highlight the therapeutic potential of anti-IL-13 antibody treatments, which are well tolerated in humans, for the treatment of pneumonia.

膳食锌缺乏症是肺炎的主要危险因素。鲍曼不动杆菌是呼吸机相关性肺炎的主要原因，也是由于多药耐药率增加而构成的严重公共卫生威胁。鲍曼不动杆菌肺炎风险增加的患者群体患锌缺乏症的风险也增加。在这里，我们建立了膳食锌缺乏症和急性鲍曼不动杆菌肺炎的小鼠模型，以检验宿主锌缺乏导致鲍曼不动杆菌发病机制的假设。我们发现，缺锌小鼠显着增加了鲍曼不动杆菌在肺部的负荷，播散到脾脏和更高的死亡率。在感染过程中，缺锌小鼠产生更多的促炎细胞因子，包括 IL-13。IL-13 的施用可促进鲍曼不动杆菌在足锌小鼠中的播散，而 IL-13 的抗体中和可保护缺锌小鼠在感染期间免受鲍曼不动杆菌的传播和死亡。这些数据强调了抗 IL-13 抗体治疗在治疗肺炎方面的潜力，这种治疗在人类中耐受性良好。