| First Author | Min-Oo G | Year | 2008 |
| Journal | Genes Immun | Volume | 9 |
| Issue | 4 | Pages | 383-8 |
| PubMed ID | 18075514 | Mgi Jnum | J:308405 |
| Mgi Id | MGI:6726694 | Doi | 10.1038/sj.gene.6364450 |
| Citation | Min-Oo G, et al. (2008) Genetic control of susceptibility to pulmonary infection with Chlamydia pneumoniae in the mouse. Genes Immun 9(4):383-8 |
| abstractText | 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. |
