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Differences in Nature Killer cell Response and Interference with Mitochondrial DNA induced Apoptosis in Moxifloxacin Environment

ABSTRACT: In light of the widespread adoption of antibiotics, the imperative to promptly manage and regulate their use, ensuring accuracy and safety, is evident. Such misuse can lead to frequent adverse drug reactions, causing unnecessary harm, and prolonged erroneous use may culminate in irreversible injuries and fatalities. Of particular concern is the prevalent use of moxifloxacin (MXF), a fourth-generation fluoroquinolone antibiotic, across various infections and disease prevention scenarios. This have been reported to have immunomodulatory effects on a variety of immune cells and even anti-proliferative and pro-apoptotic effects, but the mechanism of action is not fully clear. There exists an urgent necessity to investigate the safety and mechanisms of action on immunomodulation of this drugs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE250341 | GEO | 2024/04/15

REPOSITORIES: GEO

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Reactive oxygen species contribute to the bactericidal effects of the fluoroquinolone moxifloxacin in Streptococcus pneumoniae: metabolic pathways involved

Project description:We studied the transcriptomic response of S. pneumoniae to moxifloxacin, a fluoroquinolone that inhibits DNA gyrase. At 10 × MIC, 30 and 140 responsive genes were detected at 15 and 30 minutes, respectively. Several pathways leading to an increase in pyruvate showed up-regulation. These included 2 genes introducing P-sugars into the glycolysis and 3 out of 7 genes of the glycolysis pathway, which converts fructose-6P to pyruvate. In addition, an increase in acetyl-coA would be expected from the down-regulation of the genes coding for the acetyl-coA carboxylase, and in turn, to a further increase in pyruvate by the up-regulation of formate acetyltransferase. Since pyruvate is converted to hydrogen peroxide (H2O2) by pyruvate oxidase (SpxB), its increase would lead to an equivalent increase in the intracellular amount of H2O2, and in turn, in those of hydroxyl radicals resulting from the Fenton reaction, which damage DNA, lipids and proteins. We observed similar increases in the production of H2O2 and hydroxyl radicals under moxifloxacin treatment. These reactive oxygen species contributed to the lethality of the drug, as showed by the attenuation of its lethality in a strain lacking SpxB. These results support the production of redox alterations by fluoroquinolones and are in agreement with our previous findings showing that levofloxacin, an inhibitor of topoisomerase IV, triggers the transcriptional activation of iron transport genes. Both fluoroquinolones stimulate the Fenton reaction in their mechanism of action, by increasing the amounts of any of their two components: iron by levofloxacin or H2O2 by moxifloxacin.

2016-02-05 | GSE68947 | GEO

RNA-seq of rat Achilles tendon tissue from pefloxacin and/or dexamethasone treated animals

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Effects of Chlorogenic Acid on Hepatocytes: From Beneficial Effects to Potential Toxicity

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Gene expression data from whole lung homogenates

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