Effects of Dectin-1 on the mast cells in allergic conjunctivitis and its underlying mechanism

Our previous investigations have shown that Dectin-1 plays a crucial role in allergic conjunctivitis (AC) and the mast cells mediate this allergic reaction. Here, we tried to investigate the possible effects and underlying signal pathway of Dectin-1 on the mast cells in allergic conjunctivitis mice. 30 Balb/c mice were randomly divided into control and AC groups. The mice were immunized with phosphate buffer solution (PBS) or ovalbumin (OVA) to establish control or allergic conjunctivitis model. Prostaglandin D2 (PGD2), histamine (HIS), interleukin 4 (IL-4), and tumor necrosis factor-alpha (TNF-α) in the serum of the mice were detected using enzyme-linked immunosorbent assay (ELISA). Additionally, conjunctival tissues in mice were separated and RNA was extracted, the expression of Dectin-1 was detected using real-time PCR. Moreover, the peritoneal mast cells were separated and then stimulated using allergen OVA or control allergen BSA and mRNA levels of PGD2, histamine, IL-4 and TNF-α were detected. Furthermore, western blot was used to examine the expressions of Dectin-1, and two downstream signal molecules Syk and Bcl-10 to elucidate the possible effects and underlying mechanism of Dectin-1 on allergic conjunctivitis. The expression of Dectin-1 was significantly up-regulated in the conjunctiva tissues in AC group. Importantly, the expression of Dectin-1 in the OVA treated mast cells was dramatically elevated compared to BSA groups. Moreover, Syk and Bcl-10 were up-regulated after OVA stimulation. These data indicates that Dectin-1 via Syk-Bcl signal pathway triggers immune responses, which promotes the development of allergic conjunctivitis.