Contagious caprine pleuropneumonia (CCPP) is a highly contagious infectious disease of goats caused by Mycoplasma capricolum subspecies capripneumoniae (Mccp). CCPP outbreaks usually result in high morbidity and mortality of the affected goats, making this disease a major cause of economic losses to goat producers globally. However, the pathogenesis of CCPP remains unclear. Here, we show that IL-17-driven neutrophil accumulation is involved in the lung damage in CCPP goats. During CCPP development, intense inflammatory infiltrates could be observed in the injured lungs. Specifically, neutrophils were observed to be present within the alveoli. Increased IL-17 release drove the excessive influx of neutrophils into the lung, as IL-17 effectively stimulated the production of neutrophil chemoattractants from lung epithelial cells following Mccp infection. Our data highlight a critical role of IL-17-driven neutrophil accumulation in the pathogenesis of CCPP and suggest that IL-17 may potentially be a useful immunotherapeutic target for the treatment of CCPP.

传染性胸膜肺炎山羊（CCPP）是由山羊一种高度传染性传染病支原体山羊亚种capripneumoniae（MCCP）。CCPP爆发通常会导致受影响山羊的高发病率和高死亡率，从而使这种疾病成为全球山羊生产者经济损失的主要原因。然而，CCPP的发病机制仍不清楚。在这里，我们显示IL-17驱动的中性粒细胞积累与CCPP山羊的肺损伤有关。CCPP发生期间，在受伤的肺部可观察到强烈的炎症浸润。具体而言，观察到肺泡中存在嗜中性粒细胞。增加IL-17释放开嗜中性粒细胞的过度流入肺，如IL-17有效地激发从肺上皮细胞下面的生产嗜中性粒细胞化学引诱物的MCCP感染。我们的数据突出了IL-17驱动的中性粒细胞积累在CCPP发病机理中的关键作用，并暗示IL-17可能是治疗CCPP的潜在免疫治疗靶标。