IL-23 Contributes to Campylobacter jejuni-Induced Intestinal Pathology via Promoting IL-17 and IFNγ Responses by Innate Lymphoid Cells

Xi Jing, Anna A. Korchagina, Sergey A. Shein, Wayne T. Muraoka, Ekaterina Koroleva, Alexei V. Tumanov

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

Human pathogen Campylobacter jejuni is a significant risk factor for the development of long-term intestinal dysfunction although the cellular and molecular mechanisms remain scantily defined. IL-23 is an emerging therapeutic target for the treatment of inflammatory intestinal diseases, however its role in C. jejuni-driven intestinal pathology is not fully understood. IL-10 deficient mice represent a robust model to study the pathogenesis of C. jejuni infection because C. jejuni infection of mice lacking IL-10 results in symptoms and pathology that resemble human campylobacteriosis. To determine the role of IL-23 in C. jejuni-driven intestinal inflammation, we studied the disease pathogenesis in IL-23-/- mice with inhibited IL-10Rα signaling. These mice exhibited reduced intestinal pathology independent from bacterial clearance. Further, levels of IFNγ, IL-17, IL-22, TNF, and IL-6 were reduced and associated with reduced accumulation of neutrophils, monocytes and macrophages in the colon. Flow cytometry analysis revealed reduced production of IL-17 and IFNγ by group 1 and 3 innate lymphoid cells. Thus, our data suggest that IL-23 contributes to intestinal inflammation in C. jejuni infected mice by promoting IL-17 and IFNγ production by innate lymphoid cells.

Original languageEnglish (US)
Article number579615
JournalFrontiers in immunology
Volume11
DOIs
StatePublished - Jan 6 2021

Keywords

  • Campylobacter jejuni
  • Campylobacteriosis
  • IL-10
  • colitis
  • innate lymphoid cells
  • interleukin-23

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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