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Role of Alveolar Macrophages in Initiation and Regulation of Inflammation in Pseudomonas aeruginosaPneumonia

机译：肺泡巨噬细胞在铜绿假单胞菌肺炎的引发和炎症调节中的作用

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To evaluate the role of alveolar macrophages (AMs) in acutePseudomonas aeruginosa pneumonia in mice, AMs were depleted by aerosol inhalation of liposomes containing clodronate disodium. AM-depleted mice were then intratracheally infected with 5 × 105 CFU of P. aeruginosa. In addition to monitoring neutrophil recruitment and chemokine releases, lung injury was evaluated soon after infection (8 h) and at a later time (48 h). At 8 h, depletion of AMs reduced neutrophil recruitment, chemokine release, and lung injury. At 48 h, however, depletion of AMs decreased bacterial clearance and resulted in delayed movement of neutrophils from the site of inflammation with aggravated lung injury. With instillation of 5 × 107 CFU of bacteria, AM-depleted mice showed low mortality within 24 h of infection but high mortality at a later time, in contrast to non-AM-depleted mice. These results demonstrate that depletion of AMs has beneficial early effects but deleterious late effects on lung injury and survival in cases of P. aeruginosa pneumonia.
机译：为了评估肺泡巨噬细胞（AMs）在小鼠急性铜绿假单胞菌肺炎中的作用，通过雾化吸入含氯膦酸二钠的脂质体来消除AMs。然后用5×10 5 CFU的 P气管内感染AM缺失的小鼠。铜绿。除了监测中性粒细胞募集和趋化因子释放外，还应在感染后（8小时）和以后（48小时）评估肺损伤。在8 h，AMs的消耗减少了中性粒细胞的募集，趋化因子的释放和肺损伤。然而，在48 h，AMs的消耗减少了细菌清除，并导致中性粒细胞从炎症部位的运动延迟，并加重了肺损伤。与无AM的小鼠相比，通过注入5×10 7 CFU的细菌，AM缺失的小鼠在感染后24小时内显示出较低的死亡率，但在随后的时间内却具有较高的死亡率。这些结果表明，在 P病例中，AMs的消耗对肺损伤和生存具有有益的早期作用，但对肺损伤和存活具有有害的晚期作用。铜绿肺炎。

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