A mouse model was used to study the genetic control of differential host response to pulmonary infection with Chlamydia pneumoniae. The A/J and C57BL/6 strains show differential response to intranasal infection with respect to their ability to clear pulmonary bacterial load and the extent of lung pathology developed by 2 weeks post infection. The genetic basis of this interstrain difference was studied by whole-genome scan in an informative [A/J x C57BL/6J] F2 cross using the pulmonary microbial load as a phenotypic readout of host response. We detected a highly significant linkage (LOD score=11.5) on chromosome 17 that overlaps with the major histocompatibility (MHC) locus. This quantitative trait locus (QTL) accounts for approximately 30% of the phenotypic variance with B6 alleles conferring susceptibility and inherited in a recessive fashion. Significant linkage was also detected to chromosome 5 in female mice, while chromosome 6 showed suggestive linkage in male mice, pointing to additional complexity in the genetic control of the difference in susceptibility observed in A/J and C57BL/6J.

中文翻译：

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小鼠肺炎衣原体肺部感染易感性的遗传控制。

使用小鼠模型研究了宿主对肺炎衣原体肺感染的不同反应的遗传控制。A / J和C57BL / 6菌株在清除肺部细菌负荷的能力和感染后2周后出现的肺部病变程度方面显示出对鼻内感染的不同反应。通过全基因组扫描，在信息丰富的[A / J x C57BL / 6J] F2杂交中，使用肺微生物负荷作为宿主反应的表型读数，研究了这种菌株间差异的遗传基础。我们在与主要组织相容性（MHC）基因座重叠的17号染色​​体上检测到高度显着的连锁（LOD分数= 11.5）。该数量性状基因座（QTL）约占表型变异的30％，其中B6等位基因具有易感性并以隐性方式遗传。