Th17 cytokine profiling of colorectal cancer patients with or without enterovirus 71 antigen expression
HighlightsThe associations among EV71 infection, cytokines profiles, and CRC.Latent infection of EV71 may stimulates Th17 cells in the colorectal tumor site.Some cytokine panels have more potential in mirroring the status of virus CRC. &NA; Object. Th17 cytokines have been identified in several types of human cancers. In this pilot study, the expression of Th17 cytokines profiling in enteroviruses 71 (EV71) associated colorectal cancer (CRC) were explored. Methods 66 patients with CRC were enrolled in this study; immune‐ histochemical analyses were performed on cancerous tissues and adjacent non‐ cancerous tissues of the patients. Serum Th17 cytokines of CRC patients and healthy controls were measured using a Luminex 200 analyzer. Results Cancerous tissues had more positive EV71 antigen expression than adjacent non‐ cancerous tissues. In TNM II‐III CRC, 59.9% of cancerous tissues were observed to be EV71 positive; on the contrary, 65.2% of the adjacent non‐ cancerous epithelium was EV71 negative. In TNM I CRC, all adjacent non‐ cancerous epithelium was virus negative, but in TNM IV, half of adjacent non‐ cancerous tissues were virus positive. Serum IL‐10 were significantly higher in CRC patients than in healthy controls, and IL‐10 concentrations in the EV71 positive group were higher than those of the EV71 negative group, with the highest IL‐10 levels being observed in CRC patients with strong positive group (P < 0.05). Similar results were found for IL‐21 and IL‐23. IL‐17 levels were higher in CRC patients than in healthy controls, there was no significant difference in IL‐17 between the viral positive and viral negative groups (P > 0.05). Conclusion Persistent existing EV71 viral antigens in intestinal tissues are positively associated with TNM III/IV CRC. EV71 latent infection recruits Th17 cells in the colorectal tumor site, stimulating Th17 cytokine production that closely associated with CRC carcinogenesis.