Effect of Borrelia burgdorferi Outer Membrane Vesicles on Host Oxidative Stress Response

Wawrzeniak, Keith; Gaur, Gauri; Sapi, Eva; Senejani, Alireza G.

doi:10.3390/antibiotics9050275

Cited by 17 publications

(16 citation statements)

References 57 publications

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“…Similarly, no observable changes in cell viability were observed even after 7 days of co-culturing of B. burgdorferi with neuronal and glial cell lines [ 7 , 29 ]. A similar study further confirmed no effect on cell proliferation in neuroblastoma cells [ 30 ].…”

Section: Discussionmentioning

confidence: 57%

Effect of Invasion of Borrelia burgdorferi in Normal and Neoplastic Mammary Epithelial Cells

et al. 2021

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Borrelia burgdorferi, the causative agent of Lyme Disease, is known to be able to disseminate and colonize various organs and tissues of its hosts, which is very crucial for its pathogenicity and survival. Recent studies have shown the presence of B. burgdorferi DNA in various breast cancer tissues, in some with poor prognosis, which raises the question about whether B. burgdorferi can interact with mammary epithelial cells and could have any effect on their physiology, including tumorigenic processes. As the model in this study, we have used MCF 10A normal and MDA-MB-231 tumorigenic mammary epithelial cells and infected both cell lines with B. burgdorferi. Our immunofluorescence and confocal microscopy results showed that B. burgdorferi is capable of invading normal epithelial and breast carcinoma cell lines within 24 h; however, the infection rate for the breast carcinoma cell lines was significantly higher. While the infection of epithelial cells with B. burgdorferi did not cause any changes in cell proliferation rates, it showed a significant effect on the invasion and migratory capacity of the breast cancer cells, but not on the normal epithelial cells, as determined by Matrigel invasion and wound healing assays. We have also found that the levels of expression of several epithelial–mesenchymal transition (EMT) markers (fibronectin, vimentin, and Twist1/2) changed, with a significant increase in tissue remodeling marker (MMP-9) in MDA-MB-231 cells demonstrated by quantitative Western blot analyses. This observation further confirmed that B. burgdorferi infection can affect the in vitro migratory and invasive properties of MDA-MB-231 tumorigenic mammary epithelial cells. In summary, our results suggest that B. burgdorferi can invade breast cancer tumor cells and it can increase their tumorigenic phenotype, which urges the need for further studies on whether B. burgdorferi could have any role in breast cancer development.

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Section: Discussionmentioning

confidence: 57%

Effect of Invasion of Borrelia burgdorferi in Normal and Neoplastic Mammary Epithelial Cells

et al. 2021

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“…It was not surprising that intracellular ROS increased after radiotherapy. However, in spite of limited literature, there was still evidence showing that OMVs dramatically increased the production of MCP-1 (macrophage/monocyte chemoattractant protein-1) and MCP-2 (macrophage/monocyte chemoattractant protein-2) cytokines from neurons [ 19 ]. The elevated secretion of MCP-1 was then associated with changes in oxidative stress [ 20 , 21 ].…”

Section: Discussionmentioning

confidence: 99%

Combining Augmented Radiotherapy and Immunotherapy through a Nano-Gold and Bacterial Outer-Membrane Vesicle Complex for the Treatment of Glioblastoma

et al. 2021

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Glioblastoma, formerly known as glioblastoma multiforme (GBM), is refractory to existing adjuvant chemotherapy and radiotherapy. We successfully synthesized a complex, Au–OMV, with two specific nanoparticles: gold nanoparticles (AuNPs) and outer-membrane vesicles (OMVs) from E. coli. Au–OMV, when combined with radiotherapy, produced radiosensitizing and immuno-modulatory effects that successfully suppressed tumor growth in both subcutaneous G261 tumor-bearing and in situ (brain) tumor-bearing C57BL/6 mice. Longer survival was also noted with in situ tumor-bearing mice treated with Au–OMV and radiotherapy. The mechanisms for the successful treatment were evaluated. Intracellular reactive oxygen species (ROS) greatly increased in response to Au–OMV in combination with radiotherapy in G261 glioma cells. Furthermore, with a co-culture of G261 glioma cells and RAW 264.7 macrophages, we found that GL261 cell viability was related to chemotaxis of macrophages and TNF-α production.

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“…For example, Porphyromonas gingivalis -derived OMVs induce a shift in macrophage metabolism from oxidative phosphorylation to glycolysis, increase mitochondrial ROS production, causing pyroptotic cell death in macrophages ( Fleetwood et al, 2017 ). Borrelia burgdorferi originated-OMVs serve to directly counter superoxide production via SOD2 expression in human neuroblastoma cells ( Wawrzeniak et al, 2020 ). OMVs from Proteus mirabilis regulate the function of boar sperm via increasing ROS levels and inducing sperm membrane reconstruction ( Gao et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Role of Outer Membrane Vesicles From Helicobacter pylori in Atherosclerosis

Wang

Zhou

Chen

et al. 2021

Front. Cell Dev. Biol.

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Infection is thought to be involved in the pathogenesis of atherosclerosis. Studies have shown the association between helicobacter pylori (H. pylori) and coronary artery disease. It is interesting to find H. pylori DNA and cytotoxin-associated gene A (CagA) protein in atherosclerotic plaque. Outer membrane vesicles (OMVs), secreted by H. pylori, exert effects in the distant organ or tissue. However, whether or not OMVs from H. pylori are involved in the pathogenesis of atherosclerosis remains unknown. Our present study found that treatment with OMVs from CagA-positive H. pylori accelerated atherosclerosis plaque formation in ApoE–/– mice. H. pylori-derived OMVs inhibited proliferation and promoted apoptosis of human umbilical vein endothelial cells (HUVECs), which was also reflected in in vivo studies. These effects were normalized to some degree after treatment with lipopolysaccharide (LPS)-depleted CagA-positive OMVs or CagA-negative OMVs. Treatment with H. pylori-derived OMVs increased reactive oxygen species (ROS) levels and enhanced the activation of nuclear factor-κB (NF-κB) in HUVECs, which were reversed to some degree in the presence of a superoxide dismutase mimetic TEMPOL and a NF-κB inhibitor BAY11-7082. Expressions of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α), two inflammatory factors, were augmented after treatment with OMVs from H. pylori. These suggest that H. pylori-derived OMVs accelerate atherosclerosis plaque formation via endothelium injury. CagA and LPS from H. pylori-OMVs, at least in part, participate in these processes, which may be involved with the activation of ROS/NF-κB signaling pathway. These may provide a novel strategy to reduce the incidence and development of atherosclerosis.

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Effect of Borrelia burgdorferi Outer Membrane Vesicles on Host Oxidative Stress Response

Cited by 17 publications

References 57 publications

Effect of Invasion of Borrelia burgdorferi in Normal and Neoplastic Mammary Epithelial Cells

Effect of Invasion of Borrelia burgdorferi in Normal and Neoplastic Mammary Epithelial Cells

Combining Augmented Radiotherapy and Immunotherapy through a Nano-Gold and Bacterial Outer-Membrane Vesicle Complex for the Treatment of Glioblastoma

Role of Outer Membrane Vesicles From Helicobacter pylori in Atherosclerosis

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