Cytokine responses by conjunctival epithelial cells: An in vitro model of ocular inflammation

Salamanca, Andrés Bordalí; Calder, Virginia L.; Gao, Jianping; Galatowicz, Grazyna; Garcı́a-Vázquez, Carmen; Fernández, Itziar; Stern, Michael E.; Diebold, Yolanda; Calonge, Margarita

doi:10.1016/j.cyto.2008.07.007

Cited by 75 publications

(51 citation statements)

References 50 publications

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“…As we reported previously, TNFa or IFNc alone (for up to 72 hours) did not cause significant IOBA-NHC cell death. 35 In the current study, apoptosis was induced slightly by TNFa þ IFNc at 24 hours, and significantly after 48 hours (Fig. 4A).…”

Section: Statisticssupporting

confidence: 52%

“…35 The experimental conditions used for proinflammatory or proapoptotic stimulations are specified in the figure legends.…”

Section: Cell Culturementioning

confidence: 99%

“…Conjunctival epithelial cells including IOBA-NHC produce a plethora of cytokines and chemokines in response to TNFa and/or IFNc stimulation. 35 Desiccating stress-induced conjunctival epithelial cell apoptosis was intensified by exogenous IFNc. 14 In the next set of experiments, we investigated if inflammation has a direct role on the opening state of MPTP and, thus, may impair mitochondrial functions leading to IOBA-NHC cell apoptosis.…”

Section: Statisticsmentioning

confidence: 99%

“…The stimulatory condition used was described previously. 35 MPTP was evaluated in IOBA-NHC cells exposed to TNFa (25 ng/mL) or IFNc (500 U/mL) alone, or their combination. Ionomycin-induced MPTP opening was used as a benchmark.…”

Section: Statisticsmentioning

confidence: 99%

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Mitochondrial Permeability Transition Pore in Inflammatory Apoptosis of Human Conjunctival Epithelial Cells and T Cells: Effect of Cyclosporin A

Gao

Sana

Calder

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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RESULTS. In IOBA-NHC, TNFa, and IFNc induced MPTP opening, DWm loss, and increased cell apoptosis. This was accompanied by upregulation of Fas/FasL; Bax; and caspase-3, -8, and -9 activation. Addition of CsA prevented IOBA-NHC from cell death by blocking MPTP opening, DWm loss, Fas/FasL, and caspase activation. In PMA/aCD3-activated Jurkat T cells, MPTP opening and DWm loss were increased along with cell apoptosis and upregulated Fas/FasL/ caspase expressions. CsA further promoted T-cell apoptosis, DWm loss, and upregulation of Fas/FasL/caspase. CONCLUSIONS.Inflammation induces aberrant MPTP opening, resulting in an increased apoptosis in conjunctival epithelial cells. CsA protected IOBA-NHC from cell death by blocking both intrinsic and extrinsic apoptosis pathways. CsA promoted T-cell apoptosis via upregulating Fas/FasL and caspase activities with a minimal effect on MPTP. The findings suggest that the differential effect of CsA on T cells versus ocular surface resident epithelial cells may contribute to its therapeutic efficacy in treating ocular inflammation such as dry eye disease.

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Section: Statisticssupporting

confidence: 52%

“…35 The experimental conditions used for proinflammatory or proapoptotic stimulations are specified in the figure legends.…”

Section: Cell Culturementioning

confidence: 99%

Section: Statisticsmentioning

confidence: 99%

Section: Statisticsmentioning

confidence: 99%

See 2 more Smart Citations

Mitochondrial Permeability Transition Pore in Inflammatory Apoptosis of Human Conjunctival Epithelial Cells and T Cells: Effect of Cyclosporin A

Gao

Sana

Calder

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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“…It was previously identified that IL-1β is an important inflammatory cytokine, and participates in inflammatory responses to injury and autoimmune diseases. IL-1β, IL-6, IL-8, TNF-α and neutrophils are also involved in an autocrine loop of inflammatory mediators (19). Patients commonly develop with acute conjunctivitis as a result of bacterial or viral infections, which trigger inflammation, and cause mononuclear cells to produce high levels of IL-1β, IL-6, IL-8 and TNF-α.…”

Section: Discussionmentioning

confidence: 99%

Effects of carvedilol reduce conjunctivitis through changes in inflammation, NGF and VEGF levels in a rat model

Chen¹,

Hong²

2016

Experimental and Therapeutic Medicine

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Abstract. Carvedilol is a novel third generation β-blocker that acts as an antagonist of β and α adrenergic receptors, and is able to regulate various cell factors. In addition, it possesses antioxidant activity, is capable of reversing cardiac remodeling effects and has anti-arrhythmic effects. The present study aimed to investigate whether the effects of carvedilol were able to reduce conjunctivitis clinical scores. Initially, 24 Sprague Dawley (SD) rats were randomly divided into three equal groups as follows: Control group, model group and carvedilol group. The model and carvedilol group adult SD rats were injected with lipopolysaccharide (LPS) to induce conjunctivitis. In the carvedilol group, the eight SD rats with LPS-induced conjunctivitis also received 50 mg/kg/day of carvedilol for 4 weeks. Next, the effects carvedilol were assessed utilizing a system of clinical sign scores, and an enzyme-linked immunosorbent assay was used to determine the expression levels of interleukin-1β (IL-1β), IL-6, IL-8 and tumor necrosis factor-α (TNF-α). Finally, nuclear factor-κB (NF-κB), nerve growth factor (NGF) and vascular endothelial growth factor (VEGF) were analyzed by western blotting. Carvedilol was observed to significantly reduce clinical sign scores in a dose-dependent manner (P<0.01), and reduce IL-1β, IL-6, IL-8 and TNF-α expression levels (P<0.01) in the LPS-induced rat model of conjunctivitis. Carvedilol was also able to significantly reduce the protein expression levels of NF-κB, and induce the protein expression levels of NGF and VEGF in the LPS-induced rat model of conjunctivitis (P<0.01). In conclusion, the effects of carvedilol may reduce conjunctivitis clinical scores through inflammation, NGF and VEGF in LPS-induced rat models.

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Pathogenesis: Emphasis on Dry Eye and the Role of the Lacrimal Functional Unit in Sjögren’s Syndrome

Stern

Pflugfelder

2011

Sjögren’s Syndrome

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Cytokine responses by conjunctival epithelial cells: An in vitro model of ocular inflammation

Cited by 75 publications

References 50 publications

Mitochondrial Permeability Transition Pore in Inflammatory Apoptosis of Human Conjunctival Epithelial Cells and T Cells: Effect of Cyclosporin A

Mitochondrial Permeability Transition Pore in Inflammatory Apoptosis of Human Conjunctival Epithelial Cells and T Cells: Effect of Cyclosporin A

Effects of carvedilol reduce conjunctivitis through changes in inflammation, NGF and VEGF levels in a rat model

Pathogenesis: Emphasis on Dry Eye and the Role of the Lacrimal Functional Unit in Sjögren’s Syndrome

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