Dataset Information

Lipopolysaccharide enhances HSV-1 replication and inflammatory factor release in the ARPE-19 cells.

ABSTRACT:

Purpose

During acute retinal necrosis (ARN), retinal pigment epithelial (RPE) cells could be stimulated by both herpes simplex virus (HSV) and lipopolysaccharide (LPS). We aim to investigate the impact of LPS on HSV-1 infection and inflammatory factors in human retinal pigment epithelial cell lines (ARPE-19 cells).

Methods

ARPE-19 cells were infected by HSV-1F strain and HSVg4 strain, a modified HSV strain with GFP genes cloned in, for 1 h. Different concentrations of LPS were added. Green fluorescence protein (GFP) of HSVg4 and the infected cell protein 4 (ICP4) expression were observed. Cell culture supernatants were collected to detect 34 kinds of related cytokines and chemokines by multiplex immunoassay assay.

Results

Under LPS treatment, the cytopathic effect displayed as enlarged multinucleated cells, and the GFP fluorescence intensity and ICP4 expression increased in the HSV-1-infected ARPE-19 cells. HSV-1 infection stimulated cytokines IL-1α, IL-1β, IL-1RA, IL-2, IL-4, IL-6, IL-9, IL-12P70, IL-15, IL-18, IL-21, IL-27, TNF-α, IFN-γ and chemokines CXCL1, CXCL8, CXCL10, CXCL12, CCL2, CCL3, CCL4, CCL5, CCL11 while LPS further enhanced their expression.

Conclusion

LPS promoted HSV-1 infection and inflammatory factor release in ARPE-19 cells, indicating that ARN could deteriorate when complicated with endotoxemia.

SUBMITTER: Duan F

PROVIDER: S-EPMC9699980 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature

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Publications

Lipopolysaccharide enhances HSV-1 replication and inflammatory factor release in the ARPE-19 cells.

Duan Fang F Zeng Weiting W Zhang Yafang Y Li Dai D Wu Kaili K

Heliyon 20221121 11

<h4>Purpose</h4>During acute retinal necrosis (ARN), retinal pigment epithelial (RPE) cells could be stimulated by both <i>herpes simplex virus</i> (HSV) and lipopolysaccharide (LPS). We aim to investigate the impact of LPS on HSV-1 infection and inflammatory factors in human retinal pigment epithelial cell lines (ARPE-19 cells).<h4>Methods</h4>ARPE-19 cells were infected by HSV-1F strain and HSVg4 strain, a modified HSV strain with GFP genes cloned in, for 1 h. Different concentrations of LPS w ...[more]

PMID: 36444252

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Project description:Age related macular degeneration (AMD) is one of the leading causes of blindness. Genetics, environmental insult, and age-related factors all play a key role in altering proteostasis, the homeostatic process regulating protein synthesis, degradation and processing. These factors also play a role in the pathogenesis of AMD and it has been well established that cigarette smoking (CS) initiates AMD pathogenic mechanisms. The primary goal of this study is to elucidate whether CS can induce proteostasis/autophagy-impairment in retinal pigment epithelial (RPE) cells. In our preliminary analysis, it was found that cigarette smoke extract (CSE) induces accumulation of ubiquitinated proteins in the insoluble protein fraction (p < 0.01), which was subsequently mitigated through cysteamine (p < 0.01) or fisetin (p < 0.05) treatment. Further, it was verified that these CSE induced ubiquitinated proteins accumulated in the peri-nuclear spaces (p<0.05) that were cleared- off with cysteamine (p < 0.05) or fisetin (p < 0.05). Moreover, CSE-induced aggresome-formation (LC3B-GFP and Ub-RFP co-localization) and autophagy-flux impairment was significantly (p<0.01) mitigated by cysteamine (p<0.05) or fisetin (p<0.05) treatment, indicating the restoration of CSE-mediated autophagy-impairment. CSE treatment was also found to induce intracellular reactive oxygen species (ROS, p < 0.001) while impacting cell viability (p < 0.001), which was quantified using CMH2DCFDA-dye (ROS) and MTS (proliferation) or propodium iodide staining (cell viability) assays, respectively. Moreover, cysteamine and fisetin treatment ameliorated CS-mediated ROS production (p < 0.05) and diminished cell viability (p < 0.05). Lastly, CSE was found to induce cellular senescence (p < 0.001), which was significantly ameliorated by cysteamine (p < 0.001) or fisetin (p < 0.001). In conclusion, our study indicates that CS induced proteostasis/autophagy-impairment regulates mechanisms associated with AMD pathogenesis. Moreover, autophagy-inducing drugs such as cysteamine or fisetin can ameliorate AMD pathogenesis mechanisms that warrant further investigation in pre-clinical murine models.

Dataset Information

Lipopolysaccharide enhances HSV-1 replication and inflammatory factor release in the ARPE-19 cells.

Purpose

Methods

Results

Conclusion

Publications

Lipopolysaccharide enhances HSV-1 replication and inflammatory factor release in the ARPE-19 cells.

Similar Datasets

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