Schiøtz P O, Sørensen H, Høiby M
Acta Pathol Microbiol Scand C. 1979 Feb;87C(1):1-5.
14 cystic fibrosis (CF) patients chronically infected with mucoid P. aeruginosa and presenting multiple precipitins in serum against this bacterium (CF + P) and 13 CF patients without P. aeruginosa infection (CF-P) had their plasma and sputum sol phase examined for albumin, Clq. C3/C3c, C4 and C5 by means of electroimmunoassays. Their sputum sol phase was examined also for factor B by rocketimmunoelectrophoresis. C3c was demonstrated in the sputum sol phase but significantly more frequent (p less than 0.01) among the CF + P patients than among the CF-P patients. Factor B was also demonstrated in the sputum sol phase, but no significant difference in frequency could be demonstrated between the CF + P and the CF-P patients. None of the results indicated that a local pulmonary production of complement factors took place. Complement activation was significantly (p less than 0.01) associated with inflammation expressed as increased (formula: see text). The results show the importance of complement mediated inflammation in the pathogenesis of pulmonary tissue damage in patients with CF and support the concept of chronic P. aeruginosa lung infection as an immune complex disease in CF patients.
14名长期感染黏液型铜绿假单胞菌且血清中针对该细菌呈现多种沉淀素的囊性纤维化(CF)患者(CF + P)以及13名未感染铜绿假单胞菌的CF患者(CF - P),通过免疫电泳法检测了他们血浆和痰液液相中的白蛋白、补体C1q、C3/C3c、C4和C5。还通过火箭免疫电泳法检测了他们痰液液相中的B因子。在痰液液相中检测到了C3c,但CF + P患者中的出现频率显著高于CF - P患者(p < 0.01)。在痰液液相中也检测到了B因子,但CF + P患者和CF - P患者之间在出现频率上未显示出显著差异。没有结果表明存在局部肺组织补体因子生成。补体激活与以(公式:见原文)增加表示的炎症显著相关(p < 0.01)。结果显示补体介导的炎症在CF患者肺组织损伤发病机制中的重要性,并支持慢性铜绿假单胞菌肺部感染是CF患者免疫复合物疾病这一概念。