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Background
Although Trichinella spiralis (T. spiralis) causes zoonotic diseases, it has a strong immunomodulatory effect and has therapeutic potential for various autoimmune diseases and cancers. Our previous study results showed that T. spiralis infection can inhibit the growth of liver cancer cells, but the specific mechanism has not been elucidated.
Methods
BALB/c mice injected with H22 cells and then infected with T. spiralis were used to detect tumor inhibition rate. Cell proliferation and apoptosis of H22 cells treated with excretory-secretory product (ESP) were measured by Cell-Counting Kit 8 (CCK-8) and Flow Cytometry (FCM). The expression of apoptosis-related genes in H22 cells and tumor tissues was detected by western blotting and real-time quantitative PCR (qPCR). IL-2, IFN-γ and IL-4 production in the spleens were measured by qPCR and enzyme-linked immunosorbent assay(ELISA).
Results
The growth of tumors in tumor model mice infected with T. spiralis was significantly inhibited compared with those uninfected tumor model mice. ESP could inhibit H22 cell proliferation and induce apoptosis through the mitochondrial pathway both in vitro and in vivo. Additionally, the levels of Th1 cytokines with antitumor effects were significantly increased in the early stage of T. spiralis infection, while Th2 cytokines increased later than Th1 cytokines.
Conclusions
ESP can directly induce tumor cell apoptosis and indirectly inhibit tumor cell growth through the host immune system, which is the potential antitumor mechanism of T. spiralis infection.
Keywords
Trichinella spiralis, H22 cells, apoptosis, cytokines
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This is a preprint. It has not completed peer review.
Research
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 03 Mar, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Parasitology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Although Trichinella spiralis (T. spiralis) causes zoonotic diseases, it has a strong immunomodulatory effect and has therapeutic potential for various autoimmune diseases and cancers. Our previous study results showed that T. spiralis infection can inhibit the growth of liver cancer cells, but the specific mechanism has not been elucidated.
Methods
BALB/c mice injected with H22 cells and then infected with T. spiralis were used to detect tumor inhibition rate. Cell proliferation and apoptosis of H22 cells treated with excretory-secretory product (ESP) were measured by Cell-Counting Kit 8 (CCK-8) and Flow Cytometry (FCM). The expression of apoptosis-related genes in H22 cells and tumor tissues was detected by western blotting and real-time quantitative PCR (qPCR). IL-2, IFN-γ and IL-4 production in the spleens were measured by qPCR and enzyme-linked immunosorbent assay(ELISA).
Results
The growth of tumors in tumor model mice infected with T. spiralis was significantly inhibited compared with those uninfected tumor model mice. ESP could inhibit H22 cell proliferation and induce apoptosis through the mitochondrial pathway both in vitro and in vivo. Additionally, the levels of Th1 cytokines with antitumor effects were significantly increased in the early stage of T. spiralis infection, while Th2 cytokines increased later than Th1 cytokines.
Conclusions
ESP can directly induce tumor cell apoptosis and indirectly inhibit tumor cell growth through the host immune system, which is the potential antitumor mechanism of T. spiralis infection.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
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