Early host-pathogen interactions in the liver and spleen during systemic murine listeriosis: an overview

Abstract

Systemic listeriosis initiated by parenteral inoculation of mice with Listeria monocytogenes has been used extensively as a model infection for studying mammalian host defense against intracellular bacterial pathogens in general. Most effort has been expended on trying to understand the requirement for specific T cell-mediated immunity for combatting infection with this pathogen. By contrast, non-specific defenses have received much less attention. However, it is now obvious that these early innate defenses are critically important for the well-being of the host. If these early defenses fail to act, the murine host is rendered exquisitely susceptible to L. monocytogenes, and rapidly succumbs to overwhelming infection before T cell-mediated immunity can be generated and expressed. The most critical of these early defenses is mediated by neutrophils that rapidly accumulate in large numbers at foci of Listeria infection in the liver and spleen. These neutrophils act to curtail the growth of L. monocytogenes to levels that subsequently can be dealt with by specific defenses that are recruited into infectious foci later. In the absence of this neutrophil-mediated defense, an otherwise sublethal inoculum of L. monocytogenes rapidly grows to lethal numbers. An overview of this early aspect of murine listeriosis is presented below.