Natamycin versus voriconazole for fungal keratitis

Retamal, José; Ordenes-Cavieres, Gonzalo; Grau-Diez, Arturo

doi:10.5867/medwave.2018.08.7387

Cited by 5 publications

(1 citation statement)

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“…This may be due to the fact that inherent phagocytes residing in the corneal stroma layer can quickly recognize fungi injected into the stroma, thereby presenting antigens to activate T cells and trigger applicable immunity more quickly. Natamycin is currently the first-line drug for the treatment of FK [24][25] . As reported by others, natamycin binded to the ergosterol on the fungal cell membrane to change the permeability, which inhibited the growth of the fungus [26][27] .…”

Section: Discussionmentioning

confidence: 99%

CD3ε of a pan T cell marker involved in mouse Aspergillus fumigatus keratitis

Shi,

Yan,

Liu

et al. 2024

Int J Ophthalmol

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AIM: To explore whether CD3ε is involved in the adaptive immunity of Aspergillus fumigatus (A. fumigatus) keratitis in mice and the role of innate and adaptive immunity in it. METHODS: Mice models of A. fumigatus keratitis were established by intra-stromal injection and corneal epithelial scratching. Subconjunctival injections of natamycin, wedelolactone, LOX-1 inhibitor (poly I) or Dectin-1 inhibitor (laminarin) were used to treat mice with A. fumigatus keratitis. Mice were pretreated by intraperitoneal injection of anti-mouse CD3ε. We observed the corneal infection of mice under the slit lamp microscope and made a clinical score. The protein expression of CD3ε and interleukin-10 (IL-10) was determined by Western blotting. RESULTS: With the disease progresses, the degree of corneal opacity and edema augmented. In the intra-stromal injection models, CD3ε protein expression began to increase significantly on the 2nd day. However, in the scraping epithelial method models, CD3ε only began to increase on the 3rd day. After natamycin treatment, the degree of corneal inflammation in mice was significantly attenuated on the 3rd day. After wedelolactone treatment, the severity of keratitis worsened. And the amount of CD3ε protein was also reduced, compared with the control group. By inhibiting LOX-1 and Dectin-1, there was no significant difference in CD3ε production compared with the control group. After inhibiting CD3ε, corneal ulcer area and clinical score increased, and IL-10 expression was downregulated. CONCLUSION: As a pan T cell marker, CD3ε participate in the adaptive immunity of A. fumigatus keratitis in mice. In our mice models, the corneas will enter the adaptive immune stage faster. By regulating IL-10, CD3ε exerts anti-inflammatory and repairs effects in the adaptive immune stage.

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Section: Discussionmentioning

confidence: 99%