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Necrosis and apoptosis in Trichinella spiralis-mediated tumour reduction.

Vasilev S, Ilic N, Gruden-Movsesijan A, Vasilijic S, Bosic M, Sofronic-Milosavljevic L - Cent Eur J Immunol (2015)

Bottom Line: We found that the phenomenon could, at least partially, be related to a lower level of tumour necrosis compared to necrosis present in control animals with progressive malignancy course.ES L1 antigen, as a parasitic product that is released during the chronic phase of infection, reduced the survival and slightly, but significantly increased the apoptosis level of melanoma cells in vitro.Our results imply that powerful Trichinella anti-malignance capacity does not rely only on necrosis and apoptosis but other mechanisms through which infection or parasite products manipulate the tumor establishment and expansion should be considered.

View Article: PubMed Central - PubMed

Affiliation: Institute for the Application of Nuclear Energy - INEP, University of Belgrade, Belgrade, Serbia.

ABSTRACT
It is known that infection with different pathogens, including helminths, can alter the progression of malignant or other diseases. We studied the effect of chronic Trichinella spiralis infection or muscle larvae excretory-secretory (ES L1) antigens on the malignant tumour growth in the mouse melanoma model system in vivo and in vitro. Our results confirmed that chronic infection with T. spiralis possesses the capacity to slow down the progression of tumour growth, resulting in an impressive reduction in tumour size. We found that the phenomenon could, at least partially, be related to a lower level of tumour necrosis compared to necrosis present in control animals with progressive malignancy course. An increased apoptotic potential among the low percentage of cells within the total tumour cell number in vivo was also observed. ES L1 antigen, as a parasitic product that is released during the chronic phase of infection, reduced the survival and slightly, but significantly increased the apoptosis level of melanoma cells in vitro. Our results imply that powerful Trichinella anti-malignance capacity does not rely only on necrosis and apoptosis but other mechanisms through which infection or parasite products manipulate the tumor establishment and expansion should be considered.

No MeSH data available.


Related in: MedlinePlus

The effect of ES L1 antigen on apoptosis of mouse melanoma cells. Melanoma cells (2000 cells/well) were seeded in 24-well plates for 20 hours. Afterwards cells were treated with ES L1 antigen, stained with annexin V-FITC kit, and apoptosis was evaluated by flow cytometry. A) ES L1 in growing concentrations (50-200 μg/ml) for 72 hours; B) Time-dependent effect of ES L1 antigen on apoptosis of mouse melanoma cells determined by the treatment of cells with 200 μg/ml of ES L1 for 48 and 72 hours; C) Representative plot – 200 μg/ml of ES L1 for 72 hours. Results are presented as percentage of apoptotic cells compared to the control i.e. untreated cells (mean value ± SEM) from one out of three experiments performed in triplicate (A, B). Results are presented as the histogram of cell distribution, and a percentage of apoptotic cells from quadrant 2 and 4 are presented in quadrant 2. The presented histogram is from one representative experiment out of three with similar results (C). *p < 0.05; **p < 0.01; ##p < 0.01
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Figure 0008: The effect of ES L1 antigen on apoptosis of mouse melanoma cells. Melanoma cells (2000 cells/well) were seeded in 24-well plates for 20 hours. Afterwards cells were treated with ES L1 antigen, stained with annexin V-FITC kit, and apoptosis was evaluated by flow cytometry. A) ES L1 in growing concentrations (50-200 μg/ml) for 72 hours; B) Time-dependent effect of ES L1 antigen on apoptosis of mouse melanoma cells determined by the treatment of cells with 200 μg/ml of ES L1 for 48 and 72 hours; C) Representative plot – 200 μg/ml of ES L1 for 72 hours. Results are presented as percentage of apoptotic cells compared to the control i.e. untreated cells (mean value ± SEM) from one out of three experiments performed in triplicate (A, B). Results are presented as the histogram of cell distribution, and a percentage of apoptotic cells from quadrant 2 and 4 are presented in quadrant 2. The presented histogram is from one representative experiment out of three with similar results (C). *p < 0.05; **p < 0.01; ##p < 0.01

Mentions: Analysis of apoptosis induced by incubation of B16 melanoma cells with ES L1 antigen revealed that ES L1 antigens applied in concentrations of 100 and 200 μg/ml induced statistically significant apoptosis (p < 0.01) of mouse melanoma cells (Fig. 8A). This effect was time dependent (p < 0.01, Fig. 8B). The percentage of apoptotic B16 cells after 48 hours and 72 hours was 8.0 ±0.70% and 10.2 ±0.40% in control (un-treated) cells, while for ES L1 treated cells (200 μg/ml) it was 16.4 ±1.10% and 20.4 ±0.60%, respectively. Simultaneous staining of cells with annexin V-FITC/PI enabled detection of the intact cells, cells in early apoptosis and in late apoptosis, as well as cell death. A representative plot is showen in Fig. 8C. The obtained results indicate that treatment with ES L1 antigen induced mild apoptosis of B16 melanoma cells, which are mainly in late apoptotic phase.


Necrosis and apoptosis in Trichinella spiralis-mediated tumour reduction.

Vasilev S, Ilic N, Gruden-Movsesijan A, Vasilijic S, Bosic M, Sofronic-Milosavljevic L - Cent Eur J Immunol (2015)

The effect of ES L1 antigen on apoptosis of mouse melanoma cells. Melanoma cells (2000 cells/well) were seeded in 24-well plates for 20 hours. Afterwards cells were treated with ES L1 antigen, stained with annexin V-FITC kit, and apoptosis was evaluated by flow cytometry. A) ES L1 in growing concentrations (50-200 μg/ml) for 72 hours; B) Time-dependent effect of ES L1 antigen on apoptosis of mouse melanoma cells determined by the treatment of cells with 200 μg/ml of ES L1 for 48 and 72 hours; C) Representative plot – 200 μg/ml of ES L1 for 72 hours. Results are presented as percentage of apoptotic cells compared to the control i.e. untreated cells (mean value ± SEM) from one out of three experiments performed in triplicate (A, B). Results are presented as the histogram of cell distribution, and a percentage of apoptotic cells from quadrant 2 and 4 are presented in quadrant 2. The presented histogram is from one representative experiment out of three with similar results (C). *p < 0.05; **p < 0.01; ##p < 0.01
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4472539&req=5

Figure 0008: The effect of ES L1 antigen on apoptosis of mouse melanoma cells. Melanoma cells (2000 cells/well) were seeded in 24-well plates for 20 hours. Afterwards cells were treated with ES L1 antigen, stained with annexin V-FITC kit, and apoptosis was evaluated by flow cytometry. A) ES L1 in growing concentrations (50-200 μg/ml) for 72 hours; B) Time-dependent effect of ES L1 antigen on apoptosis of mouse melanoma cells determined by the treatment of cells with 200 μg/ml of ES L1 for 48 and 72 hours; C) Representative plot – 200 μg/ml of ES L1 for 72 hours. Results are presented as percentage of apoptotic cells compared to the control i.e. untreated cells (mean value ± SEM) from one out of three experiments performed in triplicate (A, B). Results are presented as the histogram of cell distribution, and a percentage of apoptotic cells from quadrant 2 and 4 are presented in quadrant 2. The presented histogram is from one representative experiment out of three with similar results (C). *p < 0.05; **p < 0.01; ##p < 0.01
Mentions: Analysis of apoptosis induced by incubation of B16 melanoma cells with ES L1 antigen revealed that ES L1 antigens applied in concentrations of 100 and 200 μg/ml induced statistically significant apoptosis (p < 0.01) of mouse melanoma cells (Fig. 8A). This effect was time dependent (p < 0.01, Fig. 8B). The percentage of apoptotic B16 cells after 48 hours and 72 hours was 8.0 ±0.70% and 10.2 ±0.40% in control (un-treated) cells, while for ES L1 treated cells (200 μg/ml) it was 16.4 ±1.10% and 20.4 ±0.60%, respectively. Simultaneous staining of cells with annexin V-FITC/PI enabled detection of the intact cells, cells in early apoptosis and in late apoptosis, as well as cell death. A representative plot is showen in Fig. 8C. The obtained results indicate that treatment with ES L1 antigen induced mild apoptosis of B16 melanoma cells, which are mainly in late apoptotic phase.

Bottom Line: We found that the phenomenon could, at least partially, be related to a lower level of tumour necrosis compared to necrosis present in control animals with progressive malignancy course.ES L1 antigen, as a parasitic product that is released during the chronic phase of infection, reduced the survival and slightly, but significantly increased the apoptosis level of melanoma cells in vitro.Our results imply that powerful Trichinella anti-malignance capacity does not rely only on necrosis and apoptosis but other mechanisms through which infection or parasite products manipulate the tumor establishment and expansion should be considered.

View Article: PubMed Central - PubMed

Affiliation: Institute for the Application of Nuclear Energy - INEP, University of Belgrade, Belgrade, Serbia.

ABSTRACT
It is known that infection with different pathogens, including helminths, can alter the progression of malignant or other diseases. We studied the effect of chronic Trichinella spiralis infection or muscle larvae excretory-secretory (ES L1) antigens on the malignant tumour growth in the mouse melanoma model system in vivo and in vitro. Our results confirmed that chronic infection with T. spiralis possesses the capacity to slow down the progression of tumour growth, resulting in an impressive reduction in tumour size. We found that the phenomenon could, at least partially, be related to a lower level of tumour necrosis compared to necrosis present in control animals with progressive malignancy course. An increased apoptotic potential among the low percentage of cells within the total tumour cell number in vivo was also observed. ES L1 antigen, as a parasitic product that is released during the chronic phase of infection, reduced the survival and slightly, but significantly increased the apoptosis level of melanoma cells in vitro. Our results imply that powerful Trichinella anti-malignance capacity does not rely only on necrosis and apoptosis but other mechanisms through which infection or parasite products manipulate the tumor establishment and expansion should be considered.

No MeSH data available.


Related in: MedlinePlus