A/J Mice Are Susceptible and C57BL/6 Mice Are Resistant toListeria monocytogenesInfection by Intragastric Inoculation

Abstract

Previous studies demonstrated that the innate resistance of mice to Listeria monocytogenes infection by intravenous or intraperitoneal inoculation is regulated principally by the Hc locus on mouse chromosome 2. The A/J and C57BL/6 mouse strains were identified as prototype L. monocytogenes-susceptible and -resistant strains, respectively. In the present study, we compared the relative susceptibilities of A/J and C57BL/6 mice to intragastric (i.g.) inoculation with L. monocytogenes. The results of our study indicate that A/J mice are significantly more susceptible than C57BL/6 mice to an i.g. challenge with L. monocytogenes. This was reflected in the estimated 50% lethal doses for the two strains (10 6 and 10 8 CFU for A/J and C57BL/6 mice, respectively) and a more rapid and severe dissemination of the infection to the spleen and liver in A/J mice than in C57BL/6 mice. Histopathological examination of tissues from the infected mice confirmed the greater severity of disease in A/J mice. Clearance of a primary infection enhanced the resistance of both A/J and C57BL/6 mice to reinfection with L. monocytogenes via the gastrointestinal tract. However, the relative difference in susceptibility between the two strains was evident even after immunization. The A/J mouse holds promise as a model for investigating the pathogenesis of gastrointestinal listeriosis because of its ability to develop systemic infection following challenge with numbers of organisms similar to those recovered from some L. monocytogenescontaminated food products.

Alternative Sigma Factors and Their Roles in Bacterial Virulence

“…Further, L. monocytogenes also does not appear to target the murine brain stem or the fetoplacental unit, even following intravenous injection (121,122). L. monocytogenes strains do vary in their ability to cause systemic infection in intragastrically infected mice (38), and some strains of mice (A/J) are also more susceptible than others (C57BL/6) to intragastric infection (39). However, as a consequence of the biological differences in murine and human L. monocytogenes translocation across the intestinal barrier, data from mouse infection experiments may underestimate a given strain's human virulence following oral infection.…”

Oral Inoculation of A/J Mice for Detection of Invasiveness Differences between Listeria monocytogenes Epidemic and Environmental Strains

“…Epidemic strains were significantly more invasive as a group than environmental strains and caused extensive hemorrhage in the intestines of some mice. A/J mice are relatively inefficient at mobilizing inflammatory cells, initiate a slower and less exuberant production of inflammatory cytokines, and have diminished antiListeria phagocytic activity; however, they are not considered an immunodeficient strain (6,10,14). Additionally, the macrophagemediated immune response of younger mice against L. monocytogenes infection is not fully developed (7,20).…”

“…Furthermore, studies describing intragastric infection of mice or guinea pigs required relatively high numbers of bacteria (10 9 CFU) (2,3,16,18,26). Recently, an A/J mouse model in which intragastric inoculation was used was described by Czuprynski et al (6). It was found that 6-to 8-week-old A/J mice develop systemic infection following intragastric inoculation by using numbers of organisms similar to what is detected in L. monocytogenescontaminated food products.…”

A prfA Transposon Mutant of Listeria monocytogenes F2365, a Serotype 4b Strain, Is Able To Survive in the Gastrointestinal Tract but Does Not Cause Systemic Infection of the Spleens and Livers of Intragastrically Inoculated Mice

“…It has been shown that prfA mutants are not able to invade and multiply within mammalian cells in vitro and are avirulent when inoculated intravenously or intraperitoneally into mice (6,14,15,30,33). However, there is little information regarding how prfA affects the ability of L. monocytogenes to compete and survive in the gastrointestinal (GI) tract, translocate across the intestinal mucosa, and disseminate to other organs where it can cause systemic disease.Our laboratory has developed a mouse model for gastrointestinal listeriosis in which the genetically susceptible A/J mouse strain develops significant systemic infection following peroral inoculation with L. monocytogenes at a challenge dose (i.e., approximately 10 6 CFU) that can occur in contaminated food products (8,9). In the present study, we used this model to investigate how the prfA gene affects the virulence of L. monocytogenes in the gastrointestinal tract of mice.…”

“…Our laboratory has developed a mouse model for gastrointestinal listeriosis in which the genetically susceptible A/J mouse strain develops significant systemic infection following peroral inoculation with L. monocytogenes at a challenge dose (i.e., approximately 10 6 CFU) that can occur in contaminated food products (8,9). In the present study, we used this model to investigate how the prfA gene affects the virulence of L. monocytogenes in the gastrointestinal tract of mice.…”