Cytotoxic macrophage-released tumour necrosis factor-alpha (TNF-<i>α</i>) as a killing mechanism for cancer cell death after cold plasma activation

Kaushik, Nagendra Kumar; Kaushik, Neha; Min, Booki; Choi, Ki Hong; Hong, Young June; Miller, Vandana; Fridman, Alexander; Choi, Eun Ha

doi:10.1088/0022-3727/49/8/084001

Cited by 75 publications

(57 citation statements)

References 45 publications

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“…These results suggest that intracellular ROS are responsible for plasma-induced CRT production. Tumor necrosis factor-alpha released from plasma-activated macrophages induces tumor cell death [36].…”

Section: Indirect Treatment: Plasma-assisted Cancer Immunotherapymentioning

confidence: 99%

New Hopes for Plasma-Based Cancer Treatment

Tanaka

Mizuno

Ishikawa

et al. 2018

Plasma

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Section: Indirect Treatment: Plasma-assisted Cancer Immunotherapymentioning

confidence: 99%

New Hopes for Plasma-Based Cancer Treatment

Tanaka

Mizuno

Ishikawa

et al. 2018

Plasma

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“…Plasma medical research inevitably involves experiments on reactive species because these were found to be central effectors in a number of biological targets exposed to plasma, such as skin cells [13][14][15], immune cells [16][17][18], and cancer cells . In many instances, hydrogen peroxide (H 2 O 2 ) was an important mediator in these in vitro experiments [53][54][55].…”

Section: Introductionmentioning

confidence: 99%

A Comparison of Floating-Electrode DBD and kINPen Jet: Plasma Parameters to Achieve Similar Growth Reduction in Colon Cancer Cells Under Standardized Conditions

Bekeschus

Lin

Fridman

et al. 2017

Plasma Chem Plasma Process

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A comparative study of two plasma sources (floating-electrode dielectric barrier discharge, DBD, Drexel University; atmospheric pressure argon plasma jet, kINPen, INP Greifswald) on cancer cell toxicity was performed. Cell culture protocols, cytotoxicity assays, and procedures for assessment of hydrogen peroxide (H 2 O 2 ) were standardized between both labs. The inhibitory concentration 50 (IC50) and its corresponding H 2 O 2 deposition was determined for both devices. For the DBD, IC50 and H 2 O 2 generation were largely dependent on the total energy input but not pulsing frequency, treatment time, or total number of cells. DBD cytotoxicity could not be replicated by addition of H 2 O 2 alone and was inhibited by larger amounts of liquid present during the treatment. Jet plasma toxicity depended on peroxide generation as well as total cell number and amount of liquid. Thus, the amount of liquid present during plasma treatment in vitro is key in attenuating short-lived species or other physical effects from plasmas. These in vitro results suggest a role of liquids in or on tissues during plasma treatment in a clinical setting. Additionally, we provide a platform for correlation between different plasma sources for a predefined cellular response.

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“…[29][30][31] We have reported previously the enhancement of migration and anti-tumor function of macrophages in vitro by plasma (Table 1). [32][33][34][35] In vivo effects of plasma treatment include differentiation of hemocytes in the lymph organs 48 h after plasma exposure of Drosophila melanogaster larvae, 36 but the effect of plasma activated macrophages on normal cells has not been examined.…”

Section: Introductionmentioning

confidence: 99%