HOST DEFENSES IN EXPERIMENTAL SCRUB TYPHUS - GENETICS OF NATURAL-RESISTANCE TO INFECTION
HOST DEFENSES IN EXPERIMENTAL SCRUB TYPHUS - GENETICS OF NATURAL-RESISTANCE TO INFECTION
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DOI：
10.1128/iai.19.2.583-588.1978
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发表时间：
1978-01-01
影响因子：
3.1
通讯作者：
OSTERMAN, JV
中科院分区：
文献类型：
--
作者：
GROVES, MG;OSTERMAN, JV
本文研究了30多个小鼠近交系、近交杂交种和远交种对恙虫病立克次体致死性感染的遗传抗性。用R. Gilliam株腹腔感染近交系小鼠。恙虫病有3种反应模式：敏感型（A/HeJ、C3 H/HeDub、C3 H/HeJ、C3 H/HeN、C3 H/St、CBA/J、DBA/1 J、DBA/2 J和SJL/J）、抗性型（AKR/J、BALB/cDub、BALB/cJ、C57 BL/6 J、C57 L/J和SWR/J）和选择性抗性型（A/J）。选择性耐药模式的特点是在整个滴定范围内发生随机死亡，并在调查的6只远交小鼠中的3只中观察到。近交系小鼠的H-2单倍型和它们对Gilliam感染的反应之间没有明显的相关性。5个不同抗感品种的自交系亲本杂交后代均表现为抗病。对BALB/cDub（抗性）和C3 H/HeDub（敏感）杂种F1、F2和亲本回交世代的研究表明，抗性是显性的，受单基因或紧密连锁的基因簇控制，这些基因是常染色体的，与毛色无关。BALB/cDub小鼠的耐药性不是由于宿主细胞不能支持立克次体生长，因为C3 H/HeDub和BALB/cDub胚胎细胞培养物支持Gilliam微生物的相似生长。C3 H/HeDub小鼠虽然对i. p. Gilliam感染敏感，但能够对Gilliam抗原产生免疫应答，因为s.c.感染不是致死性的，并且确实保护动物免受随后用R. Gilliam或Karp菌株的腹膜内攻击。恙虫病。
Genetic resistance to lethal infection with Rickettsia tsutsugamushi was studied in over 30 inbred strains, inbred hybrids and outbred stocks of mice. Inbred mice infected i.p. with the Gilliam strain of R. tsutsugamushi showed 3 patterns of response: susceptible (A/HeJ, C3H/HeDub, C3H/HeJ, C3H/HeN, C3H/St, CBA/J, DBA/1J, DBA/2J and SJL/J), resistant (AKR/J, BALB/cDub, BALB/cJ, C57BL/6J, C57L/J and SWR/J) and selectively resistant (A/J). The selectively resistant pattern was characterized by random deaths occurring throughout the titration range and was observed in 3 of the 6 outbred mouse stocks surveyed. No correlation was evident between the H-2 haplotype of inbred mice and their response to Gilliam infection. The progeny from 5 different Gilliam-resistant by Gilliam-susceptible inbred parental crosses were all resistant. Study of F1, F2 and parental backcross generations of BALB/cDub (resistant) and C3H/HeDub (susceptible) hybrids indicated resistance was dominant and was controlled by a single gene or a closely linked cluster of genes that were autosomal and not linked to coat color. Resistance of BALB/cDub mice was not due to an inability of host cells to support rickettsial growth, since C3H/HeDub and BALB/cDub embryo cell cultures supported similar growth of Gilliam organisms. C3H/HeDub mice, although susceptible to i.p. Gilliam infection, were capable of mounting an immune response to Gilliam antigens, since s.c. infection was not lethal and did protect animals against subsequent i.p. challenge with the Gilliam or Karp strains of R. tsutsugamushi.