HOST DEFENSES IN EXPERIMENTAL SCRUB TYPHUS - INFLAMMATORY RESPONSE OF CONGENIC C3H MICE DIFFERING AT THE RIC-GENE
HOST DEFENSES IN EXPERIMENTAL SCRUB TYPHUS - INFLAMMATORY RESPONSE OF CONGENIC C3H MICE DIFFERING AT THE RIC-GENE
复制标题
DOI：
10.1128/iai.31.3.1014-1022.1981
复制
发表时间：
1981-01-01
影响因子：
3.1
通讯作者：
OSTERMAN, JV
中科院分区：
文献类型：
--
作者：
JERRELLS, TR;OSTERMAN, JV
两种C3 H小鼠对恙虫病立克次体Gilliam株致死性感染的易感性不同。成年C3 H/RV小鼠对致死性感染的抵抗力明显高于C3 H/HeDub小鼠，并且通过混合淋巴细胞培养和移植物对主机响应。易感的C3 H/HeDub小鼠对腹膜内感染的炎症反应是明显的。感染后5天，细胞流入的幅度增加，直至动物死亡。炎症包括早期多形核白细胞反应，随后是单核细胞流入，持续至动物死亡。C3 H/RV小鼠证明了相似的细胞内流动力学，但炎症反应的幅度显著降低，C3 H/RV动物对Gilliam的反应主要是单核细胞，几乎没有多形核白细胞流入腹膜腔。如果在感染后3天给予巯基乙酸盐，则通过诱导非特异性炎症使C3 H/RV小鼠对Gilliam感染易感。用消炎痛（一种抗炎剂）治疗C3 H/HeDub小鼠，可延长Gilliam感染后的存活时间。对Gilliam的遗传抗性可能不仅仅是由于宿主对感染的反应更强，或者相反，易感性可能是由于宿主反应在数量上缺乏抗立克次体免疫所必需的细胞成分。
Two strains of C3H mice differed in their susceptibility to lethal infection with Rickettsia tsutsugamushi strain Gilliam. Adult C3H/RV mice were markedly more resistant to lethal infection than C3H/HeDub mice and both were histocompatible as assessed by mixed-lymphocyte cultures and graft-vs.-host responses. The inflammatory response of susceptible C3H/HeDub mice to intraperitoneal infection was evident .apprx. 5 days postinfection and the magnitude of the cellular influx increased until death of the animal. The inflammation consisted of an early polymorphonuclear leukocyte response, followed by a mononuclear cell influx which persisted until death of the animal. The C3H/RV mice evidenced similar kinetics of cell influx but the inflammatory response was significantly reduced in magnitude and the response of C3H/RV animals to Gilliam was predominantly mononuclear in nature, with little influx of polymorphonuclear leukocytes into the peritoneal cavity. C3H/RV mice were rendered susceptible to Gilliam infection by induction of a nonspecific inflammation with thioglycolate if given 3 days after infection. Treatment of C3H/HeDub mice with indomethacin, an anti-inflammatory agent, prolonged survival after infection with Gilliam. Genetic resistance to Gilliam may not be due simply to a greater host response to infection or, conversely, susceptibility may be due to a host response quantitatively lacking in a cellular component necessary for antirickettsial immunity.