Early translocation of acid-adapted Listeria monocytogenes during enteric infection in TNF/LTα−/− mice

Abstract

TNF/LTalpha deficient mice are devoid of Peyer's patches and lack mesenteric lymph nodes. Translocation, especially in the early steps after intragastric delivery of Listeria monocytogenes, has been explored in this study, and the role of TNFalpha has been addressed. We showed that L. monocytogenes translocation occurred at least as efficiently in TNF/LTalpha-/- mice as in TNF/LTalpha+/+ littermates. Even very low inocula (2.7x10(4) cfu) could initiate infection in the TNF/LTalpha deficient mice. Early kinetics of dissemination to the spleen and liver were similar, L. monocytogenes reaching these organs at 8 h post inoculation. However, a 10-fold higher bacterial load was observed at this early time point in the TNF/LTalpha deficient mice. rTNF pretreatment (4 h before intragastric inoculation) had no effect on the L. monocytogenes associated with the caecum-colon walls at 10 h after inoculation, although bacterial levels in the caecum-colon lumen and in spleen and liver were already controlled.

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

“…Further progress in this area has been limited in part by the general resistance of mice to listeriosis when inoculated via the GI tract. Although one report describes lethal infection in mice that were inoculated with a relatively low challenge dose via the oral route (30), most reports have described the need to use inocula of 10 8 CFU or greater to cause systemic infection following introduction of L. monocytogenes into the GI tracts of normal mice (2,6,10,16,19,22,23,25,29,33).…”

“…Murine listeriosis studies have identified some virulence determinants (23,27,31) and the importance of certain elements of innate and adaptive immune responses (4,6,10,16,24,25,29) that influence the pathogenesis of systemic listeriosis following inoculation of L. monocytogenes into the GI tract. However, the contributions of these bacterial and host factors to the pathogenesis of local versus systemic infection are incompletely understood.…”