Huang H, Potter A A, Campos M, Leighton F A, Willson P J, Haines D M, Yates W D
Department of Veterinary Pathology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon.
Can J Vet Res. 1999 Jan;63(1):69-78.
The in vitro production of proinflammatory cytokines after stimulation with Actinobacillus pleuropneumoniae and the relation of these cytokines in vivo with the disease caused by A. pleuropneumoniae were investigated. Within 24 h, in vitro stimulation by A. pleuropneumoniae (serotype 1) preparations, including killed bacteria, bacterial culture supernatant, lipopolysaccharide, and bacterial extracts, porcine pulmonary alveolar macrophages (PAM) produced significant (P < 0.05) amounts of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) as measured by bioassays. The supernatants containing interleukin-8 from PAM after stimulation by bacterial preparations showed significant neutrophil chemotaxis, while bacterial preparations alone did not. After in vivo infection with A. pleuropneumoniae, the mean levels of TNF-alpha and IL-1 in serum, as measured by bioassays, were elevated 37- to 27836-fold for TNF-alpha and 11- to 5941-fold higher for IL-1 within 4 d post-infection, depending on the treatments, and remained elevated up to Day 7. Both cytokines were also detected in porcine lungs by bioassays and immunocytochemistry. The results indicated that both secreted and surface components of A. pleuropneumoniae can stimulate PAM to produce proinflammatory mediators. Neutrophil chemoattractants rather than bacterial components are the major factor causing acute lung inflammation. The elevation of TNF-alpha and IL-1 in pigs occurred coincident with the onset of acute clinical disease.
研究了胸膜肺炎放线杆菌刺激后促炎细胞因子的体外产生情况，以及这些细胞因子在体内与胸膜肺炎放线杆菌所致疾病的关系。在24小时内，胸膜肺炎放线杆菌（血清型1）制剂，包括死菌、细菌培养上清液、脂多糖和细菌提取物，对猪肺泡巨噬细胞（PAM）进行体外刺激后，通过生物测定法测得PAM产生了大量（P < 0.05）的肿瘤坏死因子-α（TNF-α）和白细胞介素-1（IL-1）。细菌制剂刺激后的PAM含有白细胞介素-8的上清液显示出显著的中性粒细胞趋化性，而单独的细菌制剂则没有。胸膜肺炎放线杆菌体内感染后，通过生物测定法测得血清中TNF-α和IL-1的平均水平，在感染后4天内，TNF-α升高了37至27836倍，IL-1升高了11至5941倍，具体取决于治疗方法，并且一直升高到第7天。通过生物测定法和免疫细胞化学法在猪肺中也检测到了这两种细胞因子。结果表明，胸膜肺炎放线杆菌的分泌成分和表面成分均可刺激PAM产生促炎介质。中性粒细胞趋化剂而非细菌成分是导致急性肺部炎症的主要因素。猪体内TNF-α和IL-1的升高与急性临床疾病的发作同时发生。
