AI Article Synopsis
- The text discusses an opportunistic pathogen that causes vulvovaginal candidiasis (VVC) and how it utilizes lactate as a carbon source in the vaginal environment.
- It highlights that lactate can mimic the antifungal drug fluconazole (FLC) by reducing the expression of a gene responsible for ergosterol, a key component of the pathogen's membrane.
- The study suggests that the combination of lactate and FLC works synergistically, leading to the delocalization of the Cdr1 transporter, making the pathogen more susceptible to treatment.
Article Abstract
is an opportunistic pathogen that induces vulvovaginal candidiasis (VVC), among other diseases. In the vaginal environment, the source of carbon for can be either lactic acid or its dissociated form, lactate. It has been shown that lactate, similar to the popular antifungal drug fluconazole (FLC), reduces the expression of the gene and hence the amount of ergosterol in the plasma membrane. The Cdr1 transporter that effluxes xenobiotics from cells, including FLC, is delocalized from the plasma membrane to a vacuole under the influence of lactate. Despite the overexpression of the gene and the increased activity of Cdr1p, is fourfold more sensitive to FLC in the presence of lactate than when glucose is the source of carbon. We propose synergistic effects of lactate and FLC in that they block Cdr1 activity by delocalization due to changes in the ergosterol content of the plasma membrane.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8156871 | PMC |
| http://dx.doi.org/10.3390/ijms22105219 | DOI Listing |
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