Listeria monocytogenes (LM) is a Gram-positive, intracellular bacterium that can induce
spontaneous abortion,
septicemia, and
meningitis. Although it is known that neutrophils are required for elimination of the bacteria and for survival of the host, the mechanisms governing the recruitment of neutrophils to LM-infected tissues are not fully understood. We demonstrate here that
IL-23 and the
IL-17 receptor A (IL-17RA), which mediates both
IL-17A and
IL-17F signaling, are necessary for resistance against systemic LM
infection. LM-infected
IL-23p19 knockout (KO) mice have decreased production of
IL-17A and
IL-17F, while IFN-gamma production is not altered by the lack of
IL-23. LM induces the production of
IL-17A from gammadelta T cells, but not CD4, CD8, or NK cells. Furthermore, a lack of efficient neutrophil recruitment to the liver is evident in both
IL-23p19 KO and IL-17RA KO mice during LM
infection. Immunocytochemical analysis of infected livers revealed that neutrophils were able to localize with LM in
IL-23p19 KO and IL-17RA KO mice, indicating that
IL-23 and IL-17RA do not regulate the precise localization of neutrophils with LM. The importance of IL-23-induced
IL-17A was demonstrated by injecting
IL-23p19 KO mice with recombinant
IL-17A. These mice had reduced LM bacterial burdens compared with
IL-23p19 KO mice that did not receive
IL-17A. These results indicate that during LM
infection,
IL-23 regulates the production of
IL-17A and
IL-17F from gammadelta T cells, resulting in optimal liver neutrophil recruitment and enhanced bacterial clearance.