The impact of the host CCR5, TLR2 and TLR11 on production of nitric oxide, IL-6, IL-12 and growth of Toxoplasma gondii

抄録

The current study investigated the impact of the CCR5, TLR2 and TLR11 on production of nitric oxide (NO), IL-6 and IL-12 and growth of T. gondii, high virulent RH strain and avirulent PLK strain. All examined knockout macrophages infected with PLK strain produced significant lower levels of IL-12. On the other hand, TLR2- /- and TLR11-/- macrophages infected with RH strain produced significantly reduced levels of IL-12 as compared to wild-type macrophages. TLR2-/- and TLR11-/- macrophages infected with PLK strain significantly inhibited the production of IL-6 when compared to wild-type macrophages. Interestingly, significant reduction in the IL-6 and NO production was observed in TLR2-/- macrophages infected with PLK strain as compared to wild-type macrophages or to the other examined knockout macrophages. On contrary, significant increase in the NO levels was demonstrated in TLR11-/- macrophages infected with the RH strain. The growth of RH strain was significantly enhanced in CCR5-/- , TLR2-/- and TLR11-/- macrophages as compared to wild-type macrophages. The highest parasite growth of both RH and PLK strains was achieved in TLR2-/- macrophages. In conclusion, the current study suggests that TLR2 is the most critical receptor in the host defense against T. gondii infection.