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Herlinda Mejia-Lopez, Daniela Castro Farias, Victor Manuel Bautista, ; Acyclovir downregulate TNF-alpha in human limbal fibroblasts infected in vitro with Fusarium solani isolated from patient with keratitis.. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):1883.
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© ARVO (1962-2015); The Authors (2016-present)
Keratomycosis can cause damage with risk the loss of the eye. The treatment requires early and aggressive approaches based on the evolution of the lesion and the type of etiologic agent.1 In a first approach, we found the Acyclovir of inhibiting growth of Fusarium solani and Aspergillus fumigatus2 and significant decrease was ejected in MICs by amphotericin B and Natamicyn in presence of Acyclovir.3<br /> The aim of this work was to assess the expression of IL-6 and TNF-α from human limbal fibroblasts (HLF), in the presence of Fusarium solani, treated with Acyclovir, in an in vitro model.
Human limbal fibroblast from cadaveric donors were obtained and were infected with conidia of a Fusarium solani strain isolated from a patient with keratomycosis. Some were treated with Acyclovir. The expression of IL-6, TNF-α and β-actin by means of RT PCR and 2-ΔCt was evaluated.
IL-6 is expressed at similar concentrations like HLF without Acyclovir, also, infection of HLF with conidia e hyphae of F. solani, induced TNF-α expression to 4.99, and 4.6 times, respectively compared to control; while the presence of Acyclovir significantly downregulated the TNF-α expression.
To our knowledge, this is the first study to demonstrate the Acyclovir modulates the TNF-α expression from HLF infected with Fusarium solani.<br /> <br /> References. 1. Cornea 2009;28:856-859); 2.Invest Ophthalmol Vis Sci ARVO Abstract 51:E 2432; 3. Invest Ophthalmol Vis Sci. ARVO. Abstract 55:2833.
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