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Fusarium solani Activates Dectin-1 in Experimentally Induced Keratomycosis

Ling-Juan Xu1, Li-Xin Xie2

  • 1Department of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Current Medical Science
|August 4, 2018
PubMed

Insights

Dectin-1 is crucial for recognizing Fusarium solani infections in the cornea. This study shows Dectin-1 expression increases on macrophages and in infected corneas, highlighting its role in fungal keratitis.

Area of Science:

  • Immunology
  • Mycology
  • Ophthalmology

Background:

  • Fusarium solani causes fungal keratitis, a serious eye infection.
  • Dectin-1 is a pattern recognition receptor involved in innate immunity.
  • Understanding Dectin-1's role in F. solani infections is vital for developing treatments.

Purpose of the Study:

  • To investigate the role of Dectin-1 in F. solani-induced keratitis.
  • To examine Dectin-1 expression on macrophages responding to F. solani.
  • To analyze Dectin-1 and CARD9 expression patterns in a mouse model of fungal keratitis.

Main Methods:

  • Macrophages were co-cultured with F. solani spores and laminarin.
  • Dectin-1 and CARD9 expression was measured using immunofluorescence and qPCR.
  • A mouse model of fungal keratitis was created via corneal inoculation with F. solani.

Main Results:

  • Dectin-1 expression was significantly upregulated on macrophages stimulated by F. solani.
  • Dectin-1 was detected in infected corneas, with peak mRNA levels on days 2 and 3 post-infection.
  • CARD9, a downstream signaling molecule, was also upregulated in infected corneas.

Conclusions:

  • Dectin-1 plays a significant role in the host's response to F. solani keratitis.
  • The findings suggest Dectin-1 is an important recognition receptor in this fungal eye infection.
  • Further research is needed to fully elucidate the molecular mechanisms involved.
Keywords:
Dectin-1Fusarium solanikeratitis

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