HOST-PARASITE RELATIONS IN MOUSE TYPHOID
HOST-PARASITE RELATIONS IN MOUSE TYPHOID
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DOI：
10.1084/jem.124.4.573
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发表时间：
1966-01-01
影响因子：
15.3
通讯作者：
COLLINS, FM
中科院分区：
文献类型：
--
作者：
MACKANESS, GB;BLANDEN, RV;COLLINS, FM
研究了小鼠静脉感染少量链霉素敏感或耐药生物后对鼠伤寒沙门氏菌的获得性耐药性的发展。在初次感染的第14天，小鼠发展出一种机制，能够完全摧毁超感染剂量的有机体，但无法消除初次感染的有机体。后者不断地从植入部位的坏死灶回到循环中。被动转移主动感染或接种的动物的血清，以及用热灭活的生物体免疫，提高了宿主从血液中清除生物体的能力，但不会对它们随后在组织中的繁殖造成任何重大干扰。结果表明，活动性感染动物的抵抗力依赖于一种非体液机制，该机制能够从内源或外源破坏生物。
The development of acquired resistance to Salmonella typhimurium has been studied in mice infected intravenously with small numbers of streptomycin-sensitive or streptomycin-resistant organisms. By the 14th day of a primary infection the mouse develops a mechanism capable of destroying completely a super infecting dose of organisms, but is unable to eliminate organisms of the primary infection. The latter are constantly returned to the circulation from necrotic foci at the sites of implantation. Passive transfer of serum from actively infected or vaccinated animals, and immunization with heat-killed organisms, increase the capacity of the host to clear organisms from the blood, but do not interfere to any significant extent with their subsequent multiplication in the tissues. It is concluded that the resistance of actively infected animals depends on a nonhumoral mechanism capable of destroying organisms from endogenous or exogenous sources.