Re-infection with liver fluke, Opisthorchis viverrini, increases proinflammatory molecules involved in
inflammation-mediated disease and
carcinogenesis in an animal model. To clarify whether these genes respond to parasite
antigen in peripheral blood leukocytes (PBL) of
opisthorchiasis patients, we examined the transcriptional level of
oxidant-generating (
toll-like receptor 2 (TLR-2),
nuclear factor-kappa B (
NF-KB), and
cyclooxygenase 2 (COX-2)),
anti-oxidant-generating (
manganese superoxide dismutase 2 (SOD-2) and
catalase (CAT)), proinflammatory
cytokine (interleukin (IL)-1β), and anti-inflammatory
cytokine (IL-10), in PBL exposed to parasite
antigen in O. viverrini-infected patients compared with healthy individuals in an in vitro experiment. After O. viverrini
antigen-treated PBL, quantitative RT-PCR analysis revealed that increased expression of
cytokines and
oxidant-generating genes in PBL was similar between O. viverrini-infected and healthy groups. Interestingly, compared with healthy subjects, increase of TLR-2, COX-2, and SOD-2 and decreased CAT
mRNA expression levels were observed in O. viverrini-infected group. The results indicate that O. viverrini
antigen induces upregulation of TLR-2, COX-2, and SOD-2 and downregulation of CAT genes in
opisthorchiasis patients, suggesting that imbalance of
oxidant/
anti-oxidant transcripts during
re-infection may be involved in the inflammatory-driven
carcinogenesis. These molecules may be used as the chemopreventive target for intervention of
opisthorchiasis patients in an endemic area.