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Interleukin-10 Gene Therapy-Mediated Amelioration of Bacterial Pneumonia

机译：白介素10基因治疗介导的细菌性肺炎改善

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Respiratory infection by Actinobacillus pleuropneumoniae causes a highly pathogenic necrotizing pleuropneumonia with severe edema, hemorrhage and fever. Acute infection is characterized by expression of inflammatory cytokines, including interleukin-1 (IL-1), IL-6 and IL-8. To determine if high level production of inflammatory cytokines contributed to disease pathogenesis, we investigated if inhibiting macrophage activation with adenovirus type 5-expressed IL-10 (Ad-5/IL-10) reduced the severity of acute disease. Porcine tracheal epithelial cells infected with Ad-5/IL-10 produced bioactive human IL-10. When pigs were intratracheally infected with A. pleuropneumoniae, pigs pretreated with Ad-5/IL-10 showed a significant reduction in the amount of lung damage when compared to adenovirus type 5-expressing β-galactosidase (Ad-5/β-Gal)-treated and untreated pigs. In addition, serum zinc levels were unchanged, the lung weight/body weight ratio (an indicator of vascular leakage) was significantly reduced, and lung pathology scores were reduced. Myeloperoxidase activity in lung lavage fluid samples, an indicator of neutrophil invasion, was decreased to levels similar to that seen in pigs not infected withA. pleuropneumoniae. Reduction in inflammatory cytokine levels in lung lavage fluid samples correlated with the clinical observations in that pigs pretreated with Ad-5/IL-10 showed a corresponding reduction of IL-1 and tumor necrosis factor (TNF) compared with untreated and Ad-5/β-Gal-treated pigs. IL-6 levels were unaffected by pretreatment with Ad-5/IL-10, consistent with observations that IL-6 was not derived from alveolar macrophages. Since inflammatory cytokines are expressed at high levels in acute bacterial pleuropneumonia, these results indicate that macrophage activation, involving overproduction of IL-1 and TNF, is a prime factor in infection-related cases of massive lung injury.
机译：胸膜肺炎放线杆菌的呼吸道感染可引起高致病性坏死性胸膜肺炎，并伴有严重的水肿，出血和发烧。急性感染的特征是表达炎症性细胞因子，包括白介素-1（IL-1），IL-6和IL-8。为了确定炎症细胞因子的高水平产生是否导致疾病发病，我们调查了用表达5型腺病毒的IL-10（Ad-5 / IL-10）抑制巨噬细胞活化是否降低了急性疾病的严重程度。用Ad-5 / IL-10感染的猪气管上皮细胞产生具有生物活性的人IL-10。当猪气管内感染 A时。胸膜肺炎，经Ad-5 / IL-10预处理的猪与未经治疗的表达5型腺病毒的β-半乳糖苷酶（Ad-5 /β-Gal）相比，肺损伤程度显着降低猪。此外，血清锌水平未改变，肺重/体重比（血管渗漏的指标）显着降低，肺病理评分降低。肺灌洗液样本中的髓过氧化物酶活性（嗜中性粒细胞浸润的指标）降低至与未感染emA的猪相似的水平。胸膜肺炎。肺灌洗液样品中炎性细胞因子水平的降低与临床观察结果相关，与未治疗和Ad-5 / IL-10相比，经Ad-5 / IL-10预处理的猪表现出相应的IL-1和肿瘤坏死因子（TNF）降低。 β-Gal处理的猪。用Ad-5 / IL-10预处理不会影响IL-6水平，这与观察到的IL-6并非来自肺泡巨噬细胞有关。由于炎性细胞因子在急性细菌性胸膜肺炎中高水平表达，因此这些结果表明，与感染相关的大规模肺损伤病例中的主要因素是巨噬细胞活化，包括IL-1和TNF的过度产生。

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