Giebink G S, Dee T H, Kim Y, Quie P G
Infect Immun. 1980 Sep;29(3):1062-6. doi: 10.1128/iai.29.3.1062-1066.1980.
Pneumococcal opsonic activity and concentrations of pneumococcal capsular polysaccharide antigen, C3, C4 factor B, C3 and factor B breakdown products were measured in the serum obtained acutely from 12 patients with serious pneumococcal disease. One patient showed markedly reduced pneumococcal opsonic activity, borderline-low C3, and the presence of C3 and factor B breakdown products and died. Although eight additional patients showed depressed levels of C3 or C4 or the presence of C3 or factor B breakdown products, none had reduced pneumococcal opsonic activity. All of the three remaining patients had normal opsonic activity and C3 and C4 levels. Covalescent serum was obtained from eight patients; six had normal C3 and C4 levels, and two had persistent C4 depression. These data show that complement is activated during pneumococcal disease and suggest that extensive complement activation may impair pneumococcal opsonic activity in certain patients and thereby compromise an important host defense mechanism.
对12例重症肺炎球菌病患者急性期采集的血清进行了肺炎球菌调理活性、肺炎球菌荚膜多糖抗原、C3、C4、B因子、C3及B因子降解产物浓度的检测。1例患者肺炎球菌调理活性显著降低,C3处于临界低水平,存在C3及B因子降解产物,最终死亡。另外8例患者虽C3或C4水平降低,或存在C3或B因子降解产物,但均无肺炎球菌调理活性降低。其余3例患者的调理活性及C3、C4水平均正常。8例患者采集了恢复期血清;6例C3、C4水平正常,2例C4持续降低。这些数据表明,肺炎球菌病期间补体被激活,提示广泛的补体激活可能损害某些患者的肺炎球菌调理活性,从而损害一种重要的宿主防御机制。