Resistance and susceptibility of mice to bacterial infection: genetics of listeriosis

Abstract

A survey of various strains of mice showed distinct differences in resistance or susceptibility to Listeria monocytogenes. C57B1, related sublines, NZB, and SJL were resistant to Listeria, whereas BALB/c, CBA, A, DBA/1, C3H, LP.RIII, 129, and WB were susceptible. The gene(s) responsible for resistance and susceptibility to Listeria were studied in detail. C57B16/6, BMO.D2, and B1O.A mice were 100 times more resistant than were BALB/c, CBA, and A. Resistance of the (C57B1/6 x BALB/c)F1 was intermediate between the two parents, suggesting partial penetration of a dominant gene. Backcross studies in which the (C57B1/6 x ratories at the Austin Hospital or the Microbiology Department by strict brother-sister mating. The mice were mostly derived from the Jackson Laboratory, Bar Harbor, Me. (from the colonies of M. Cherry, G.

Functional deficiencies of peritoneal cells from gene-targeted mice lacking G-CSF or GM-CSF

“…It was surprising to note that there was no deficiency in the 24-h granulopoietic response in the peritoneal cavity of either strain after intraperitoneal infection, but both GM-CSF Ϫ/Ϫ and G-CSF Ϫ/Ϫ mice were deficient in their 3-day macrophage inflammatory response. Such a deficiency in numbers of cells in the peritoneal cavity could well account for the susceptibility to infection because the Lsr gene that governs natural variation in resistance or susceptibility of mouse strains to Listeria has been linked to the efficiency of this inflammatory response [7,8]. However, possible differences in the activity of end cells present during infection could also contribute to the increased susceptibility of the knockout mice.…”

“…Soon after injection, the bacteria are engulfed by resident macrophages. The genetic resistance of some strains of mice [7] relates to a rapid inflammatory response in the first 48 h of infection [8], which appears to be governed by the numbers of hemopoietic cells in bone marrow and spleen [9]. Acquired immunity rests largely on activation of macrophage bactericidal ability [10] but depletion studies using monoclonal antibody to the Gr1 granulocyte marker have shown that granulocytes are also required both in the primary and secondary infections [11].…”

Genetic control of susceptibility of mice to infection with E. histolytica

“…For this reason, and because the putative gene is not linked to the major histocompatibility complex, it is presumably controlling some function associated with natural (innate) resistance to amoebiasis, rather than being associated with specific immune mechanisms. Thus, it resembles the genes controlling natural resistance to other organisms such as Listeria monocytogenes (Cheers & McKenzie 1978), Salmonella typhimurium (Plant and Glynn 1976), Leishmania donovani (Bradley 1977), Myobacterium bovis (Skamene et al 1982), and viral infection (Haller, Arnheiter & Lindenmann 1980). Unlike these genes, however, susceptibility rather than resistance is dominant in this case, and it is not yet known at what level or through what cell type this gene operates.…”

New Data, Strategies, and Insights for Listeria monocytogenes Dose‐Response Models: Summary of an Interagency Workshop, 2011

“…(39,40) Notably, laboratory animal strains differ in susceptibility to infection, likely due to some genetic susceptibility determinants, and disruptions of the immune system that result in Tcell deficiencies can markedly increase susceptibility to infection. (46)(47)(48)(49)(50)(51)(52)(53)(54) For example, both major histocompatibility complex (MHC) I and MHC II deficient knock-out mice are clearly more susceptible to infection than wild-type mice. (54) The traditional experimental endpoint for mice is septicemic death, expressed as LD 50 , the dose required to cause death in 50% of animals.…”