Production of interleukin-1β related to mammalian target of rapamycin/Toll-like receptor 4 signaling pathway during infection of the mouse cornea.

AIM

To elucidate the effect of rapamycin on regulating the production of interleukin (IL)-1β in ()-induced keratitis and to verify whether the expression of IL-1β in keratitis is associated with the mammalian target of rapamycin (mTOR)/Toll-like receptor 4 (TLR4) signaling pathway.

METHODS

Fungal keratitis mouse models of susceptible C57BL/6 mice were established using . The mice were subsequently treated with rapamycin. The protein levels of p-mTOR, TLR4, and IL-1β in normal and infected corneal tissue were measured by Western blot. The TLR4 and IL-1β mRNA levels were determined by real-time polymerase chain reaction (PCR).

RESULTS

In C57BL/6 mice, rapamycin treatment decreased the clinical scores and production of the pro-inflammatory cytokine, IL-1β. The expression of TLR4, stimulated by , was reduced as well when the mTOR signaling pathway was suppressed by rapamycin.

CONCLUSION

Rapamycin is beneficial for the outcome of fungal keratitis and has an inhibitory effect expression of the inflammatory cytokine IL-1β. The inhibitory effect on IL-1β expression can be associated with the mTOR/TLR4 signaling pathway in infection in mice.