Non-specific resistance mechanisms to listeriosis: implications for experimental and naturally occurring infection

Use of murine listeriosis as an experimental model has greatly increased our understanding of the complex interplay of cells and mediators in non-specific antibacterial resistance (innate immunity). Important contributions made with this experimental model include demonstrating the ability of inflammatory cytokines (i.e. IFN-gamma, IL-1 alpha, TNF-alpha) to protect against bacterial infection, and illustrating the rapidity of the host cytokine response (detectable within 1 h of challenge) during bacterial infection. Most experimental studies of host defense against Listeria monocytogenes (L. monocytogenes) have used a parenteral challenge (i.v. or i.p.). This ignores the pathogenesis of naturally occurring listeriosis, which usually results from ingestion of Listeria-contaminated food products. In this review, we will include consideration of the host-pathogen interactions that occur when L. monocytogenes invades through its natural portal of entry, the gastrointestinal tract. Although resistance to facultative intracellular pathogens, such as L. monocytogenes, was formerly thought to revolve exclusively around the T helper cell/macrophage axis, more recent evidence indicates that neutrophils are able to ingest and kill L. monocytogenes and prevent the unrestricted multiplication of listeriae in parenchymal cells. Exploring the mechanisms involved in this process will provide new insights into the communication between leukocytes and tissue cells in host defense.