The role of Mincle in innate immune to fungal keratitis

Abstract

Introduction: This study aimed to detect the early expression of macrophage-inducible C-type lectin (Mincle) and investigate its role in the innate immune response of fungal keratitis (FK). Methodology: Wistar rats were used to make fungal keratitis models. The inflammatory responses and corneal lesions were observed by slitlamp microscope.RT-PCR, immunohistochemistry, and immunofluorescence were used to detect the expression of Mincle in the rat corneal epithelium. The expression of eight cytokines (CXCL1, CXCL2, IL-1β, IL-6, IL-10, TNF-α, CCL2, CCL3) were detected by real-time RT-PCR and immunohistochemistry. Lastly, corneal epithelium of 54 patients with Aspergillus fumigatus keratitis and 13 ocular trauma patients were collected to detect expression of Mincle by real-time RT-PCR, and 12 FK and 10 ocular trauma paraffin samples were collected to confirm expression of Mincle by immunohistochemistry. Results: The expression of Mincle was significantly upregulated at 4, 8, 16, and 24 hours after fungal infection. There were significant differences in the expression of the eight inflammatory cytokines between the blank control group and the fungus-infected group. Mincle expression was correlated with the expression of TNF-a, IL-1β, IL-10, and CCL3 in the cornea. The mRNA expressions of Mincle in the corneas of both normal and FK patients were significantly different. Conclusions: The expression of Mincle increases significantly during the early period of Aspergillus fumigatus infection, while expression of eight corresponding cytokines changes. Mincle, as a pattern recognition receptor, may play a role in the early innate immune response of the corneal resistance against fungus.

Differential susceptibility of Dectin‐1 isoforms to functional inactivation by neutrophil and fungal proteases

“…Similar to Dectin-1–induced responses, Dectin-2–mediated responses are blocked by the presence of the RodA layer on resting conidia ( 12 ). Whereas Mincle expression is up-regulated in response to A. fumigatus stimulation ( 16 ), a role for Mincle during the response to A. fumigatus has not been identified to date ( 17 ). In agreement with these data, we observed that A. fumigatus SC-induced TNF from Biogel-elicited inflammatory monocytes/macrophages was partially dependent on Dectin-1 and Dectin-2, but independent of Mincle.…”

Perillaldehyde AmelioratesAspergillus fumigatusKeratitis by Activating the Nrf2/HO-1 Signaling Pathway and Inhibiting Dectin-1-Mediated Inflammation

“…Their diameter was 3 mm and they were made of colorless, translucent, and nontoxic sealing film Parafilm M (BEMIS, Sheboygan Falls, WI, USA) with 127 µm thick. 32 , 33 Parafilm M has good ductility, unique permeability, excellent moisture permeability, and strong corrosion resistance. The eyelids were sutured after soft contact lenses were worn for prevention of further fungi leakage.…”

The C-Type Lectin Mincle: Clues for a Role in Crohn’s Disease Adjuvant Reaction

“…Factors that were also documented in literature related to Crohn’s disease are depicted in bold. References of the different ligands not mentioned in the text are for bacterial pathogen species ( 11 – 13 ), Leishmania ( 14 ), mycobacteria, and corynebacteria ( 15 , 16 ), Streptococcus pneumonia ( 17 ), Helicobacter pylori ( 18 ), Malassezia ( 19 , 20 ), Aspergillus fumigatus ( 21 ), Candida albicans ( 22 , 23 ), SAP130 ( 10 , 24 , 25 ), β-glucosylceramide ( 26 ), cholesterol crystals ( 27 ), and cholesterol sulfate ( 28 ). References for the various signaling molecules not mentioned in the text are for TLR4/MyD88 ( 29 ), PKC ( 30 ), vav proteins ( 31 ), HIF1α ( 32 ) and Nlrp3 ( 33 , 34 ).…”