| First Author | Gervais F | Year | 1984 |
| Journal | J Immunol | Volume | 132 |
| Issue | 4 | Pages | 2078-83 |
| PubMed ID | 6699408 | Mgi Jnum | J:7345 |
| Mgi Id | MGI:55816 | Doi | 10.4049/jimmunol.132.4.2078 |
| Citation | Gervais F, et al. (1984) Genetic control of resistance to Listeria monocytogenes: regulation of leukocyte inflammatory responses by the Hc locus. J Immunol 132(4):2078-83 |
| abstractText | The control mechanisms responsible for the innate resistance of C57BL/6J (B) mice and for the innate susceptibility of A/J (A) mice to infection with Listeria monocytogenes were studied by typing the recombinant inbred (RI) strains derived from these two progenitors for the trait of Listeria resistance/susceptibility. The strain distribution pattern (SDP) of this trait obtained in the 13 AXB/BXA RI strains studied suggests that an allelic difference at a major locus (Lr-1) is responsible for the trait of resistance/susceptibility to Listeria. In addition, another putative gene (Lr-2) unlinked to Lr-1 is postulated to control the level of bacterial load within the group of susceptible strains. The SDP of A and B alleles at the Lr-1 locus was fully concordant with that observed for the Hc locus (controlling the level of the C5 component of complement). This suggests that the genetic susceptibility of A strains of mice to Listeria infection is either directly due to or related to the C5 deficiency found in that strain. This conclusion is enhanced by the observation of a significant protection of A mice from listeriosis by the infusion of C5-rich serum. A survey of RI strains for the magnitude of PMN and macrophage inflammatory responses showed that the expression of both traits co-segregated and that the C5 deficiency was the major factor responsible for the defective inflammatory response of A strain mice. We conclude that a defect in the phagocyte inflammatory responses caused by C5 deficiency is the major reason for the extreme susceptibility of A mice to Listeria. |
