A Novel Innate Response of @entity1 Corneal Epithelium to Heat-killed XXXX by Producing Peptidoglycan Recognition Proteins.

@entity1 @entity9651 @entity2348 @entity5132 @entity281 @entity364 @entity59218 @entity30462
UNASSIGNED: @entity364 of the cornea can be sight-threatening and have a worse prognosis than other types of microbial @entity281 . Peptidoglycan recognition proteins (PGLYRP), which are expressed on the ocular surface, play an important role in the immune response against @entity2348 by activating toll-like receptors (TLRs) or increasing phagocytosis. However, the role of PGLYRPs in innate immune response to fungal pathogens has not been investigated. In this study, we observed a significant induction of three PGLYRPs 2-4 in primary @entity1 corneal epithelial cells (HCECs) exposed to live or heat-killed @entity5132 (HKCA). The C-type lectin receptor @entity9651 plays a critical role in controlling @entity5132 infections by promoting phagocytic activity and cytokine production in macrophages and dendritic cells. Here, we demonstrate that @entity9651 is expressed by normal @entity1 corneal tissue and primary HCECs. HKCA exposure increased expression of @entity9651 on HCECs at mRNA and protein levels. Interestingly, @entity9651 neutralizing antibody, IkB-a inhibitor @entity30462 , and NF-kB activation inhibitor @entity59218 blocked NF-kB p65 nuclear translocation, as well as the induction of the PGLYRPs by HKCA in HCECs. Furthermore, rhPGLYRP-2 was found to suppress colony-forming units of @entity5132 in vitro. In conclusion, these findings demonstrate that @entity9651 is expressed by @entity1 corneal epithelial cells, and @entity9651 /NF-kB signaling pathway plays an important role in regulating @entity5132 /HKCA-induced PGLYRP secretion by HCECs.
