Temporal Transcriptomic Profiling Reveals DECTIN-1–Mediated Immune Responses in Acanthamoeba Keratitis

Abstract

Purpose The purpose of this study was to investigate the dynamic immune response and the role of DECTIN-1 in Acanthamoeba keratitis (AK). Methods The AK mouse model was established, and corneal tissue samples were collected at 1, 3, and 7 days post-infection (dpi). Transcriptomic profiling was performed to analyze differentially expressed genes and enriched Gene Ontology terms. Immune cell infiltration was estimated using ImmuCellAI-mouse. The expression of DECTIN-1 and associated signaling molecules was validated using quantitative PCR, immunostaining, and Western blotting. In vitro experiments were conducted to assess DECTIN-1 expression in human corneal epithelial cells (HCECs). Results AK progression was characterized by dynamic changes, with peak inflammatory responses at 3 dpi. Immune infiltration analysis revealed early innate immune activation followed by adaptive immune involvement at later stages. Temporal transcriptome analysis identified DECTIN-1 as a significantly upregulated gene throughout disease progression. Activation of the DECTIN-1/SYK/NF-κB signaling pathway was associated with increased expression of pro-inflammatory cytokines. In vitro experiments confirmed that Acanthamoeba directly induced DECTIN-1 expression in HCECs. Conclusions DECTIN-1 was dynamically upregulated during AK and may play a potential role in mediating innate immune responses and shaping immune cell dynamics. These findings provided new insights into AK pathogenesis and indicated DECTIN-1 as a potential therapeutic target.