Yersin B R, Glauser M P, Freedman L R
Infect Immun. 1982 Jan;35(1):320-5. doi: 10.1128/iai.35.1.320-325.1982.
Cellular host defenses are considered to be ineffective in bacterial endocarditis; the microorganisms in infected vegetations are protected from phagocytic cells by dense layers of fibrin. To test this hypothesis, nitrogen mustard-induced agranulocytosis and leukopenia were produced in rabbits with right-sided streptococcal endocarditis. The spontaneous sterilization of tricuspid infection observed in the control animals was not present in the granulocytopenic, leukopenic animals. Since the bacterium Streptococcus intermedius is not sensitive to the complement-mediated bactericidal effect of serum and since the animals were not bacteremic during the time of agranulocytosis, an inhibitory effect of the drug on local cellular host defense mechanisms is postulated. We suggest that the spontaneous sterilization of infective endocarditis in the right side of the heart in rabbits is mediated by cellular host defenses.
细胞宿主防御在细菌性心内膜炎中被认为是无效的；感染赘生物中的微生物被致密的纤维蛋白层保护，免受吞噬细胞的侵害。为了验证这一假设，在患有右侧链球菌性心内膜炎的兔子中诱导产生了氮芥引起的粒细胞缺乏症和白细胞减少症。在粒细胞减少、白细胞减少的动物中未观察到对照动物中出现的三尖瓣感染的自发清除。由于中间链球菌对血清补体介导的杀菌作用不敏感，且在粒细胞缺乏期间动物没有菌血症，因此推测该药物对局部细胞宿主防御机制有抑制作用。我们认为，兔子心脏右侧感染性心内膜炎的自发清除是由细胞宿主防御介导的。
