Grover G J, Loegering D J
Circ Shock. 1984;14(1):39-47.
Previous studies from this laboratory have shown that thermal injury can cause sufficient intravascular hemolysis to depress reticuloendothelial system (RES) phagocytic function and that the injection of red blood cell (RBC) stroma depresses RES function and increases susceptibility to experimental shock. The present study evaluated the effect of thermal injury and RBC stroma on susceptibility to infection with Streptococcus pneumoniae as well as the effect of RBC stroma on the RES clearance and killing of the bacteria. The mortality rate following pneumococcal infection was increased after thermal injury from 0% to 100% (P less than .01), and with the injection of RBC stroma (0.5 ml/100 g) mortality increased from 20% to 80% (P less than .01). Hepatic uptake of heat-killed S. pneumoniae was depressed from 64% to 44% of the injected dose following the injection of RBC stroma. RBC stroma depressed complement CH50 levels by 31%. The reduction in the number of viable S. pneumoniae present in the liver between 30 min and 4 hr following bacterial challenge was decreased in animals receiving RBC stroma. This was interpreted as an indication of impaired hepatic bactericidal function and was associated with an increase in the number of circulating viable S. pneumoniae. It is concluded that the increased susceptibility to pneumococcal infection induced by RBC stroma was probably due to an impairment in hepatic clearance and killing of the bacteria. The depressed bacterial clearance could have been contributed to by the stroma-induced decrease in complement levels. This study further supports the hypothesis that the intravascular hemolysis caused by thermal injury contributes to the increased susceptibility to infection following this form of injury.
本实验室先前的研究表明,热损伤可导致足够的血管内溶血,从而抑制网状内皮系统(RES)的吞噬功能,并且注射红细胞(RBC)基质会抑制RES功能并增加对实验性休克的易感性。本研究评估了热损伤和RBC基质对肺炎链球菌感染易感性的影响,以及RBC基质对RES清除和杀灭细菌的影响。热损伤后肺炎球菌感染后的死亡率从0%升至100%(P<0.01),注射RBC基质(0.5 ml/100 g)后死亡率从20%升至80%(P<0.01)。注射RBC基质后,肝脏对热灭活肺炎链球菌的摄取量从注射剂量的64%降至44%。RBC基质使补体CH50水平降低了31%。在接受RBC基质的动物中,细菌攻击后30分钟至4小时肝脏中存活的肺炎链球菌数量的减少幅度降低。这被解释为肝脏杀菌功能受损的迹象,并与循环中存活的肺炎链球菌数量增加有关。结论是,RBC基质诱导的对肺炎球菌感染易感性增加可能是由于肝脏对细菌的清除和杀灭功能受损。基质诱导的补体水平降低可能导致了细菌清除能力下降。本研究进一步支持了以下假设:热损伤引起的血管内溶血导致这种形式的损伤后感染易感性增加。