Mycoplasma infection of cultured cells induces oxidative stress and attenuates cellular base excision repair activity

Ji, Yunhee; Karbaschi, Mahsa; Cooke, Marcus S.

doi:10.1016/j.mrgentox.2019.05.010

Cited by 21 publications

(20 citation statements)

References 21 publications

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“…We could abundantly find sequences of Mycoplasma DnaK early in infected mice, while only a low amount of copy number was found in primary and secondary tumors, pointing to a “hit and run/hide” mechanism [ 168 ]. Given the fact that infections with certain Mycoplasmas lead to ROS production [ 49 , 178 ], and ROS can cause direct damage to DNA, our data provide a molecular link between a Mycoplasma protein, DnaK, and cellular transformation.…”

Section: Mycoplasmas and Cancermentioning

confidence: 87%

Mycoplasmas–Host Interaction: Mechanisms of Inflammation and Association with Cellular Transformation

2020

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Mycoplasmas are the smallest and simplest self-replicating prokaryotes. Located everywhere in nature, they are widespread as parasites of humans, mammals, reptiles, fish, arthropods, and plants. They usually exhibiting organ and tissue specificity. Mycoplasmas belong to the class named Mollicutes (mollis = soft and cutis = skin, in Latin), and their small size and absence of a cell wall contribute to distinguish them from other bacteria. Mycoplasma species are found both outside the cells as membrane surface parasites and inside the cells, where they become intracellular residents as “silent parasites”. In humans, some Mycoplasma species are found as commensal inhabitants, while others have a significant impact on the cellular metabolism and physiology. Mollicutes lack typical bacterial PAMPs (e.g., lipoteichoic acid, flagellin, and some lipopolysaccharides) and consequently the exact molecular mechanisms of Mycoplasmas’ recognition by the cells of the immune system is the subjects of several researches for its pathogenic implications. It is well known that several strains of Mycoplasma suppress the transcriptional activity of p53, resulting in reduced apoptosis of damaged cells. In addition, some Mycoplasmas were reported to have oncogenic potential since they demonstrated not just accumulation of abnormalities but also phenotypic changes of the cells. Aim of this review is to provide an update of the current literature that implicates Mycoplasmas in triggering inflammation and altering critical cellular pathways, thus providing a better insight into potential mechanisms of cellular transformation.

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Section: Mycoplasmas and Cancermentioning

confidence: 87%

Mycoplasmas–Host Interaction: Mechanisms of Inflammation and Association with Cellular Transformation

2020

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“…DNA was extracted using a QIAamp DNA mini kit (Qiagen, Manchester, UK), and quantified using a NanoDrop One (Thermo Fisher Scientific, Waltham, MA, USA), prior to quantitative PCR analysis, as described below. For the ELISA, cells were exposed to 50 µM H 2 O 2 for 30 min, on ice, (as described elsewhere [59]) before DNA was extracted, and ELISA performed, as referenced below.…”

Section: Methodsmentioning

confidence: 99%

Genome-Wide Adductomics Analysis Reveals Heterogeneity in the Induction and Loss of Cyclobutane Thymine Dimers across Both the Nuclear and Mitochondrial Genomes

Alhegaili

Sylvius

et al. 2019

IJMS

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The distribution of DNA damage and repair is considered to occur heterogeneously across the genome. However, commonly available techniques, such as the alkaline comet assay or HPLC-MS/MS, measure global genome levels of DNA damage, and do not reflect potentially significant events occurring at the gene/sequence-specific level, in the nuclear or mitochondrial genomes. We developed a method, which comprises a combination of Damaged DNA Immunoprecipitation and next generation sequencing (DDIP-seq), to assess the induction and repair of DNA damage induced by 0.1 J/cm2 solar-simulated radiation at the sequence-specific level, across both the entire nuclear and mitochondrial genomes. DDIP-seq generated a genome-wide, high-resolution map of cyclobutane thymine dimer (T<>T) location and intensity. In addition to being a straightforward approach, our results demonstrated a clear differential distribution of T<>T induction and loss, across both the nuclear and mitochondrial genomes. For nuclear DNA, this differential distribution existed at both the sequence and chromosome level. Levels of T<>T were much higher in the mitochondrial DNA, compared to nuclear DNA, and decreased with time, confirmed by qPCR, despite no reported mechanisms for their repair in this organelle. These data indicate the existence of regions of sensitivity and resistance to damage formation, together with regions that are fully repaired, and those for which > 90% of damage remains, after 24 h. This approach offers a simple, yet more detailed approach to studying cellular DNA damage and repair, which will aid our understanding of the link between DNA damage and disease.

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“…Mycoplasma infection is a cause for serious concern in cell culture laboratories; it is difficult to detect or treat, and leads to anomalous cell behaviour. Among its detrimental effects, as shown by Ji et al [4], are the induction of DNA damage -both strand breaks and oxidised bases (detected with hOGG1, the human counterpart of Fpg) -and a serious delay in the repair of oxidised bases.…”

Section: Methodsmentioning

confidence: 99%

Introduction to hCOMET special issue, ‘Comet assay in vitro’

Dušinská

Costa

Collins

2019

Mutation Research/Genetic Toxicology and Environmental Mutagene

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Mycoplasma infection of cultured cells induces oxidative stress and attenuates cellular base excision repair activity

Cited by 21 publications

References 21 publications

Mycoplasmas–Host Interaction: Mechanisms of Inflammation and Association with Cellular Transformation

Mycoplasmas–Host Interaction: Mechanisms of Inflammation and Association with Cellular Transformation

Genome-Wide Adductomics Analysis Reveals Heterogeneity in the Induction and Loss of Cyclobutane Thymine Dimers across Both the Nuclear and Mitochondrial Genomes

Introduction to hCOMET special issue, ‘Comet assay in vitro’

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