scholarly journals Co-regulation of Dectin-1 and TLR2 in inflammatory response of human corneal epithelial cells induced by Aspergillus fumigates

2016 ◽  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial ◽  
Aspergillus Fumigates ◽  
Human Corneal Epithelial Cells

scholarly journals Impact of Mycotoxins Secreted by Aspergillus Molds on the Inflammatory Response of Human Corneal Epithelial Cells

Toxins ◽  
2017 ◽  
Vol 9 (7) ◽  
pp. 197 ◽  
Author(s):  
Yélian Bossou ◽  
Youssra Serssar ◽  
Amel Allou ◽  
Sandrine Vitry ◽  
Isabelle Momas ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial ◽  
Human Corneal Epithelial Cells

scholarly journals Anandamide Concentration-Dependently Modulates Toll-Like Receptor 3 Agonism or UVB-Induced Inflammatory Response of Human Corneal Epithelial Cells

2021 ◽  
Vol 22 (15) ◽  
pp. 7776
Author(s):  
Ágnes Angyal ◽  
Zsófia Pénzes ◽  
Shahrzad Alimohammadi ◽  
Dorottya Horváth ◽  
Lili Takács ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Toll Like Receptor ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial ◽  
Uvb Irradiation ◽  
Human Corneal Epithelial Cells ◽  
Anti Inflammatory

Photodamage-induced and viral keratitis could benefit from treatment with novel nonsteroid anti-inflammatory agents. Therefore, we determined whether human corneal epithelial cells (HCECs) express members of the endocannabinoid system (ECS), and examined how the endocannabinoid anandamide (AEA, N-arachidonoyl ethanolamine) influences the Toll-like receptor 3 (TLR3) agonism- or UVB irradiation-induced inflammatory response of these cells. Other than confirming the presence of cannabinoid receptors, we show that endocannabinoid synthesizing and catabolizing enzymes are also expressed in HCECs in vitro, as well as in the epithelial layer of the human cornea in situ, proving that they are one possible source of endocannabinoids. p(I:C) and UVB irradiation was effective in promoting the transcription and secretion of inflammatory cytokines. Surprisingly, when applied alone in 100 nM and 10 μM, AEA also resulted in increased pro-inflammatory cytokine production. Importantly, AEA further increased levels of these cytokines in the UVB model, whereas its lower concentration partially prevented the transcriptional effect of p(I:C), while not decreasing the p(I:C)-induced cytokine release. HCECs express the enzymatic machinery required to produce endocannabinoids both in vitro and in situ. Moreover, our data show that, despite earlier reports about the anti-inflammatory potential of AEA in murine cornea, its effects on the immune phenotype of human corneal epithelium may be more complex and context dependent.

scholarly journals Influence of Pseudomonas autoinducer N-3-oxododecanoyl homoserine lactone on human corneal epithelial cells

2020 ◽  
pp. 153537022096983
Author(s):  
Renjian Hu ◽  
Kelan Yuan ◽  
Jie Zhou ◽  
Yue Zhang ◽  
Jiao Zheng ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Homoserine Lactone ◽  
Host Cells ◽  
Time Dependent ◽  
Cell Counting ◽  
Dependent Manner ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial ◽  
Human Corneal Epithelial Cells

The quorum-sensing (QS) signaling-dependent extracellular virulence factors of Pseudomonas aeruginosa can cause infections such as P. aeruginosa keratitis. P. aeruginosa communicates by secreting and sensing small chemical molecules called autoinducers in QS system. The key QS signal molecule, N-3-oxododecanoyl-homoserine lactone (3OC12HSL), can affect the behavior of host cells and initiate immune response. In this report we investigated the influence of 3OC12HSL on human corneal epithelial cells (HCECs) and the mechanisms of 3OC12HSL on activated toll-like receptor 2 (TLR2)-dependent interleukin-8 (IL-8) secretion in HCECs. Cells were cultured under different concentrations of 3OC12HSL. Cell viability was assessed using Crystal violet staining and the cell counting kit-8 assay. We demonstrated the administration of 3OC12HSL decreased HCEC viability and survival in a concentration- and time-dependent manner. At high concentrations, 3OC12HSL rapidly promoted a time-dependent increase in the expressions of TLR2 and TLR4. It was found that the nuclear translocation and expression of nuclear factor-κB (NF-κB) were also increased in response to 3OC12HSL treatment. The significantly elevated expressions of TLR2, TLR4, and NF-κB, encouraged us to further test their mechanisms that cause inflammatory response. Among the inflammatory factors examined (IL-6, IL-8, IL-10, and TNF-α), we found that IL-8 was significantly increased after treatment with 3OC12HSL and its expression was inhibited when TLR2 was specifically blocked or silenced. These results indicated that the QS signaling molecule 3OC12HSL could be recognized by the host innate immune system in HCECs. This recognition then triggered an immune inflammatory response involving the activation of TLR2 and an increase in expression of IL-8. This crosstalk between 3OC12HSL and host immunity in HCECs contributes to the development and progression of P. aeruginosa keratitis.

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