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Regulatory effect of caspase-11 on interleukin-1β in the fungal keratitis

Keke Zhu1, Hongmei Mu1, Baimu Pi1

  • 1Department of Ophthalmology, Kaifeng Central Hospital, Kaifeng, Henan Province, China.

Pakistan Journal of Pharmaceutical Sciences
|February 8, 2017
PubMed

Insights

Fungal keratitis involves interleukin-1 beta (IL-1β) production by neutrophils. Caspase-11 regulates IL-1β maturation via Caspase-1, independent of TLR4/TRIF and NLRP3 inflammasomes.

Area of Science:

  • Ophthalmology
  • Immunology
  • Mycology

Background:

  • Fungal keratitis is a severe corneal infection causing blindness, particularly in developing countries.
  • Interleukins are key proinflammatory cytokines in corneal immune defense against fungal pathogens.
  • The cellular sources and regulatory pathways of interleukin expression in fungal keratitis remain unclear.

Purpose of the Study:

  • To investigate the role of Caspase-11 in regulating Interleukin-1 beta (IL-1β) during fungal keratitis.
  • To identify the specific cell types involved in IL-1β production in the cornea.
  • To elucidate the signaling pathways governing IL-1β synthesis and maturation in fungal keratitis.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) and Western blotting were employed.
  • Caspase-11 was cultured and analyzed.
  • Investigated the involvement of TLR4/TRIF, Dectin-1/Syk pathways, and inflammasomes (NLRP3, ASC) in IL-1β generation.

Main Results:

  • Neutrophils are the primary source of IL-1β in corneal innate antifungal immunity.
  • IL-1β generation was induced by fungal infection, not via classical pre-excitation pathways.
  • The Dectin-1/Syk pathway, but not TLR4/TRIF, was involved in IL-1β generation.
  • Caspase-1 and Caspase-11 were crucial for IL-1β maturation, with Caspase-11 regulating Caspase-1 processing.
  • NLRP3 and ASC inflammasomes were not implicated in IL-1β generation.

Conclusions:

  • Neutrophils are key effector cells for IL-1β production in fungal keratitis.
  • IL-1β maturation is regulated by the Caspase-1/Caspase-11 axis, modulated by the Dectin-1/Syk pathway.
  • Specific signaling pathways like TLR4/TRIF and NLRP3 inflammasome are not involved in IL-1β precursor generation.

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