Innate and adaptive immune responses during listeria monocytogenes infection

Mammalian hosts have multiple, redundant ways to rapidly respond to the presence of infection. These innate immune mechanisms are triggered within minutes to hours after infection. Although they are not microbe specific, they do contribute to limiting exponential growth of L. monocytogenes and may even reduce bacterial dissemination to secondary infection sites. The role of these rapid immune responses can be clearly demonstrated by examining bacterial loads in various inbred strains of laboratory mice, with CFU burdens differing by 100- to 1,000-fold within the first few days of infection (1, 2). This difference has been attributed largely to multiple innate immune mechanisms, and both the prototypic susceptible strain (BALB/c) and highly resistant C57BL/6 mice can induce robust CD8⁺ T cell responses and eventually clear sublethal doses of L. monocytogenes. Weak or delayed innate immunity allows L. monocytogenes to replicate exponentially for several days and thus is a major determinant of disease severity. The innate immune responses generated during the first few days of infection are also critical for proper induction of the adaptive immune mechanisms that lead to immunological memory (3-5).