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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Susceptibility to tuberculosis: A locus on mouse chromosome 19 (Trl-4) regulates Mycobacterium tuberculosis replication in the lungs
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Susceptibility to tuberculosis: A locus on mouse chromosome 19 (Trl-4) regulates Mycobacterium tuberculosis replication in the lungs

机译：肺结核易感性：小鼠第19号染色体（Trl-4）上的一个基因位点调节肺结核分枝杆菌的复制

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The mouse DBA/2 (D2) strain is very susceptible to infection with virulent Mycobacterium tuberculosis, whereas C57BL/6 (B6) is much more resistant. Infection of D2 and B6 mice with M. tuberculosis H37Rv by the respiratory route is biphasic: during the first 3 weeks, there is rapid bacterial growth in the lung of both strains, whereas beyond this point replication stops in B6 but continues in D2, causing rapidly fatal pulmonary disease. To identify the genes regulating growth of M. tuberculosis in the lungs of these two strains, 98 informative (B6 x D2) F-2 mice were infected by the respiratory route with M. tuberculosis H37Rv (2 x 10(2) colony-forming units), and the extent of bacterial replication in the lungs at 90 days was used as a quantitative measure of susceptibility in a whole-genome scan. Quantitative trait locus mapping identified a major locus on chromosome 19 (Tuberculosis resistance locus-4, Trl-4; logarithm of odds 5.6), which regulated pulmonary replication of M. tuberculosis and accounted for 25% of the phenotypic variance. B6 alleles at Trl-4 were inherited in an incompletely dominant fashion and associated with reduced bacterial replication. An additional effect of a locus (Trl-3), previously shown to affect survival to i.v. infection with M. tuberculosis, was also noted. F2 mice homozygous for B6 alleles at both Trl-3 and Trl-4 were as resistant as B6 parents, whereas mice homozygous for D2 alleles were as susceptible as D2 parents. These results suggest a strong genetic interaction between Trl-3 and Trl-4 in regulating pulmonary replication of M. tuberculosis. [References: 61]
机译：小鼠DBA / 2（D2）株极易感染强力结核分枝杆菌，而C57BL / 6（B6）更具有抵抗力。 D2和B6小鼠通过呼吸道感染结核分枝杆菌H37Rv是双相的：在最初的3周中，两种品系的肺部都有快速的细菌生长，而超过这一点，在B6中复制停止，但在D2中继续复制，从而导致快速致命的肺部疾病。为了鉴定调节这两株肺中结核分枝杆菌生长的基因，通过呼吸道感染了98例（B6 x D2）F-2小鼠，感染了结核分枝杆菌H37Rv（2 x 10（2））单位），并将90天时肺中细菌复制的程度用作全基因组扫描敏感性的定量度量。数量性状基因座作图鉴定了19号染色体上的一个主要基因座（结核病抗性基因座4，Trl-4；对数为5.6），它调节了结核分枝杆菌的肺复制，占表型变异的25％。 Trl-4的B6等位基因以不完全优势的方式遗传，并与细菌复制减少有关。先前显示可影响到i.v.的生存的基因座（Trl-3）的附加作用。还注意到结核分枝杆菌感染。 Trl-3和Trl-4的B6等位基因纯合的F2小鼠与B6亲本一样具有抗性，而D2等位基因纯合的小鼠与D2亲本一样易感。这些结果表明在调节结核分枝杆菌的肺复制中，Tr-1-3和Tr-1-4之间有很强的遗传相互作用。 [参考：61]

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