Collins F M, Scott M T
Infect Immun. 1974 May;9(5):863-9. doi: 10.1128/iai.9.5.863-869.1974.
The growth of Salmonella enteritidis in mice pretreated with 700 mug of killed Corynebacterium parvum was less than that seen in normal CD-1 mice. In treated mice, there was an early increased inactivation of the blood, liver, and spleen bacterial populations, followed by a prolonged period of slow but continuous bacterial growth. The treated mice failed to develop significant delayed hypersensitivity and did not show the characteristic antibacterial immune response seen in untreated infected animals. Eventually sufficient resistance did develop in most of the treated animals to protect them against the lethal effects of the challenge infection. The peak C. parvum effect was seen when S. enteritidis was injected 7 to 14 days later. Injection of C. parvum 24 h after the bacterial challenge actually potentiated the Salmonella infection. There was no evidence of an increased specific humoral response by the C. parvum-treated mice, suggesting that the slower growth of the S. enteritidis was due to the continued enhanced killing of the bacterial population by the nonspecifically stimulated cells of the reticuloendothelial system, rather than to any specific augmentation of the host immune response.
用700微克灭活的微小棒状杆菌预处理的小鼠中,肠炎沙门氏菌的生长低于正常CD-1小鼠。在处理过的小鼠中,血液、肝脏和脾脏中的细菌群体早期失活增加,随后是一段延长的缓慢但持续的细菌生长时期。处理过的小鼠未能产生显著的迟发型超敏反应,也未表现出未处理的感染动物中所见的特征性抗菌免疫反应。最终,大多数处理过的动物确实产生了足够的抵抗力,以保护它们免受激发感染的致死作用。当肠炎沙门氏菌在7至14天后注射时,微小棒状杆菌的效果达到峰值。在细菌攻击后24小时注射微小棒状杆菌实际上增强了沙门氏菌感染。没有证据表明微小棒状杆菌处理的小鼠有增加的特异性体液反应,这表明肠炎沙门氏菌生长较慢是由于网状内皮系统非特异性刺激的细胞对细菌群体的持续增强杀伤,而不是由于宿主免疫反应的任何特异性增强。