FCN-A mediates the inflammatory response and the macrophage polarization in Aspergillus fumigatus keratitis of mice by activating the MAPK signaling pathway.

Abstract

Fungal keratitis (FK) is a severe corneal disease that may cause vision loss. Previous studies indicate that the innate immune response produces the most effective anti-Aspergillus immune resistance. Ficolin-A (FCN-A), a soluble pattern-recognition receptor (PRR) family plays an important role in the innate immunity. In this study, we aimed to study the role of FCN-A in the A. fumigatus infected cornea. Here for the first time, we reported that the expression of FCN-A increases after A. fumigatus infection in the cornea of mice. Then, our results showed that the down-regulation of FCN-A reduced the inflammatory response of the cornea infected mice and decreased the expression of the TNF-a, p-p38, p-JNK. We also found that FCN-A can affect the recruitment of macrophages in the cornea of mice with A. fumigatus keratitis. In the mouse model of A. fumigatus keratitis and the A. fumigatus stimulation of RAW 264.7 cells, knocking down of FCN-A expression promoted the macrophage polarization toward M2. Furthermore, we observed that both the p38 and JNK inhibitors pretreatment decreased the proportion of M1/M2 in RAW 264.7 cells. Taken together, our data provide evidence that FCN-A participated in the inflammatory response of A. fumigatus keratitis in mice. Moreover, FCN-A mediates the inflammatory response and the polarization of the macrophages by activating the MAPK signaling pathway in A. fumigatus keratitis.