Abstract

Listeria monocytogenes (LM) is a gram‐positive, intracellular bacterium that induces the secretion of pro‐inflammatory cytokines, IL‐12 and IL‐18. LM strains either deficient in listeriolysin O (LLO−LM) or deficient in LLO but replaced with an alternate hemolysin, perfringolysin, tagged for proteasome degradation (LLO−PFO+PEST) have enhanced our ability to understand the secretion of IL‐12 and IL‐18 during cytoplasmic or noncytoplasmic invasion of LM. It is unknown which innate immune cells are secreting IL‐12 and IL‐18 during different stages of LM infection; however, we have found that neutrophils are secreting predominantly more IL‐12 one day after infection with LM. Neutrophils are associated with LM in the periarteriolar lymphoid sheath (PALS) by one day post infection. Infection of mice with LLO−LM does not induce migration of infected cells into the PALS at one day post infection whereas this migration is induced during infection with LLO−PFO+PEST LM. Interestingly, neither mutant strain induces IL‐12 or IL‐18 secretion. Studies are currently ongoing to determine how this localization is induced and whether these mutant strains can induce protective immunity.

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