The Role of the IL-23/IL-17 axis and neutrophils during infection with Listeria monocytogenes

Date of Award


Degree Type


Degree Name

Doctor of Philosophy


Graduate School of Biomedical Sciences

First Advisor

Rance Berg, Ph.D


Infection with the gram-positive, intracellular bacteria, Listeria monocytogenes (LM) induces a pro-inflammatory cytokine environment and inflammatory cell influx to sites of infection. The cytokine IL-23 is involved in the maintenance of IL-17A and IL-17F secreting cells which are indirectly required for the recruitment of neutrophils during infection. Neutrophils are thought to be essential for resistance against LM infection; however, their specific role during LM Infection has yet to be defined. By using knockout mice that are deficient in IL-23 or the IL-17 receptor-A, thus devoid of IL-17A and IL-17F signaling, we demonstrate a protective role for the IL-23/IL-17 axis during infection with LM. Our data suggest that the IL-23/IL-17 axis can regulate the continual recruitment of neutrophils into the liver. Furthermore, we demonstrate a protective role for neutrophils. Neutrophils can produce TNF-α, but not IFN-γ during LM infection. Collectively, these data indicate that the IL-23/IL-17 axis and neutrophils are required for resistance against LM infection

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