IL-22 production is regulated by IL-23 during Listeria monocytogenes Infection but is not required for Bacterial clearance or tissue protection

Amy C. Graham, Karen D. Carr, Amy N. Sieve, Mohanalaxmi Indramohan, Timothy J. Break, Rance E. Berg

Research output: Contribution to journalArticle

30 Scopus citations

Abstract

Listeria monocytogenes (LM) is a gram-positive bacterium that is a common contaminant of processed meats and dairy products. In humans, ingestion of LM can result in intracellular infection of the spleen and liver, which can ultimately lead to septicemia, meningitis, and spontaneous abortion. Interleukin (IL)-23 is a cytokine that regulates innate and adaptive immune responses by inducing the production of IL-17A, IL-17F, and IL-22. We have recently demonstrated that the IL-23/IL-17 axis is required for optimal recruitment of neutrophils to the liver, but not the spleen, during LM infection. Furthermore, these cytokines are required for the clearance of LM during systemic infection. In other infectious models, IL-22 induces the secretion of anti-microbial peptides and protects tissues from damage by preventing apoptosis. However, the role of IL-22 has not been thoroughly investigated during LM infection. In the present study, we show that LM induces the production of IL-22 in vivo. Interestingly, IL-23 is required for the production of IL-22 during primary, but not secondary, LM infection. Our findings suggest that IL-22 is not required for clearance of LM during primary or secondary infection, using both systemic and mucosal models of infection. IL-22 is also not required for the protection of LM infected spleens and livers from organ damage. Collectively, these data indicate that IL-22 produced during LM infection must play a role other than clearance of LM or protection of tissues from pathogen- or immune-mediated damage.

Original languageEnglish
Article numbere17171
JournalPLoS ONE
Volume6
Issue number2
DOIs
StatePublished - 2011

Fingerprint Dive into the research topics of 'IL-22 production is regulated by IL-23 during Listeria monocytogenes Infection but is not required for Bacterial clearance or tissue protection'. Together they form a unique fingerprint.

  • Cite this