Objective To explore the mechanism of miR-214 in immunoregulation of type II alveolar cells infected by Mycobacterium tuberculosis. Methods A549 cells were infected with BCG and H37Rv. qRT-PCR was used to measure the expression levels of miR-214 and FGF9. Western blot was used to measure the expression level of FGF9. SP- A, SP-D, TLR2, TLR4, IL-10, TNF-α, TNF-γ, IL-1β and IL-8 were measure by ELISA. Western blot was used to detect expression of PI3K, AKT and p-AKT. Results Compared with those in cells infected with BCG, expression of miR-214 was increased, and expression of FGF9 was decreased in A549 cells infected with H37Rv. Compared with those in the NC- mimic+oe-NC group, SP-A, SP-D and IL-10 were decreased significantly, TLR2, TLR4, TNF-α, TNF-γ, IL-1β and IL-8 were increased significantly. PI3K and AKT/ p-AKT expression was increased significantly in the miR-214-mimic+oe-NC group, SP-A, SP-D and IL-10 were increased significantly. TLR2, TLR4, TNFα, TNF-γ, IL-1 β and IL-8 were decreased significantly, PI3K and AKT/ p-AKT expression was decreased significantly in the NC mimic+oe-FGF9 group. Compared with those in the NC-mimic+oe-NC group, SP-A, SP-D and IL-10 were increased significantly, TLR2, TLR4, TNF-α, TNF-γ, IL-1 β and IL-8 were decreased significantly. PI3K and AKT/ p-AKT expression was decreased significantly in the miR-214 mimic+oe-FGF9 group. Conclusions miR-214 inhibits FGF9 expression and activates the PI3K/ AKT signaling pathway, which leads to the excessive immune response of type II alveolar cells infected by Mtb and the development of inflammation.