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Effect of glucose supplementation on human bronchial epithelial cells infected with Cryptococcus neoformans
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Abstract
Diabetes could be a risk factor for cryptococcal meningitis in immunocompetent individuals. A model frequently used to understand cellular changes in diabetes consists of exposure to high concentrations of glucose in vitro. In the airways, epithelial cells are crucial for the establishment of cryptococcosis. We evaluated the effects of the combination of Cryptococcus neoformans and glucose concentrations (at 5mM or 15mM) on human bronchial epithelial cells (BEAS-2B) for 24h. No cytotoxic effect was observed in cells stimulated by C. neoformans and/or treated with glucose supplementation. C. neoformansincreased IL-6 and IL-8 productions and NF-kB, ERK1/2 and STAT3 activations in BEAS-2B cells when compared to control. In contrast to increased IL-6 production and STAT3 activation the IL-8 production and ERK1/2 activation markedly decreased upon culturing of cells stimulated by C. neoformans and supplemented by glucose when compared to cells only infected with C. neoformans. In addition, the glucose supplementation increased the internalization of C. neoformans in cells but reduced the percentage of C. neoformans on the surface and its growth. Conclusion: The glucose supplementation promoted pro- and anti-inflammatory responses in bronchial epithelial cells infected with C. neoformans.
Title: Effect of glucose supplementation on human bronchial epithelial cells infected with Cryptococcus neoformans
Description:
Abstract
Diabetes could be a risk factor for cryptococcal meningitis in immunocompetent individuals.
A model frequently used to understand cellular changes in diabetes consists of exposure to high concentrations of glucose in vitro.
In the airways, epithelial cells are crucial for the establishment of cryptococcosis.
We evaluated the effects of the combination of Cryptococcus neoformans and glucose concentrations (at 5mM or 15mM) on human bronchial epithelial cells (BEAS-2B) for 24h.
No cytotoxic effect was observed in cells stimulated by C.
neoformans and/or treated with glucose supplementation.
C.
neoformansincreased IL-6 and IL-8 productions and NF-kB, ERK1/2 and STAT3 activations in BEAS-2B cells when compared to control.
In contrast to increased IL-6 production and STAT3 activation the IL-8 production and ERK1/2 activation markedly decreased upon culturing of cells stimulated by C.
neoformans and supplemented by glucose when compared to cells only infected with C.
neoformans.
In addition, the glucose supplementation increased the internalization of C.
neoformans in cells but reduced the percentage of C.
neoformans on the surface and its growth.
Conclusion: The glucose supplementation promoted pro- and anti-inflammatory responses in bronchial epithelial cells infected with C.
neoformans.
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