IL-17 plays a central role in initiating experimental Candida albicans infection in mouse corneas

Hongbo Zhang, Hongxia Li, Yuanyuan Li, Yanli Zou, Xiaomeng Dong, Wengang Song, Changkai Jia, Siyuan Li, Haijie Xi, Dongmin Liu, Yiqiang Wang*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

30 Citations (Scopus)

Abstract

The pathogenesis of fungal infection in the cornea remains largely unclear. To understand how the immune system influences the progression of fungal infection in corneas, we inoculated immunocompetent BALB/c mice, neutrophil- or CD4+ T-cell-depleted BALB/c mice, and nude mice with Candida albicans. We found that only immunocompetent BALB/c mice developed typical Candida keratitis (CaK), while the other mouse strains lacked obvious clinical manifestations. Furthermore, CaK development was blocked in immunocompetent mice treated with anti-IL-17A or anti-IL-23p19 to neutralize IL-17 activity. However, no significant effects were observed when Treg cells, γδ T cells, or IFN-γ were immunodepleted. Upon infection, the corneas of BALB/c mice were infiltrated with IL-17-producing leukocytes, including neutrophils and, to a lesser degree, CD4+ T cells. In contrast, leukocyte recruitment to corneas was significantly diminished in nude mice. Indeed, nude mice produced much less chemokines (e.g. CXCL1, CXCL2, CXCL10, CXCL12, CCL2, and IL-6) in response to inoculation. Remarkably, addition of CXCL2 during inoculation restored CaK induction in nude mice. In contrast to its therapeutic effect on CaK, neutralization of IL-17 exacerbated Candida-induced dermatitis in skin. We conclude that IL-17, mainly produced by neutrophils and CD4+ T cells in the corneas, is essential in the pathogenesis of CaK.

Original languageEnglish
Pages (from-to)2671-2682
Number of pages12
JournalEuropean Journal of Immunology
Volume43
Issue number10
DOIs
Publication statusPublished - Oct 2013
Externally publishedYes

Keywords

  • Candida albicans
  • Corneal infection
  • Fungal infection
  • IL-17
  • Neutrophil

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