Pathways of Corneal and Ocular Surface Inflammation: A Perspective from the Cullen Symposium

McDermott, Alison M.; Pérez, Víctor L.; Huang, Andrew J.W.; Pflugfelder, Stephen C.; Stern, Michael E.; Baudouin, Christophe; Beuerman, Roger W.; Burns, Alan R.; Calder, Virginia L.; Calonge, Margarita; Chodosh, James; Coster, Douglas J.; Dana, Reza; Hazlett, Linda D.; Jones, Dan B.; Kim, Stella K.; Knop, Erich; Li, De Quan; Mitchell, Bradley M.; Niederkorn, Jérry Y.; Pearlman, Eric; Wilhelmus, Kirk R.; Kurie, Elaine

doi:10.1016/s1542-0124(12)70238-0

Cited by 49 publications

(39 citation statements)

References 3 publications

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“…There was a significant difference between provoked and unprovoked eye for the same cytokines: IL-6, IFNγ, and IL-10 (86) . We speculate that individuals exposed to air pollution or other hazardous stimuli can elicit the similar inflammatory cascade during acute phase and lead to EDED clinical presentation, similar to other ocular surface inflammatory diseases, such as AKC (78) . Goblet cell hyperplasia results from exposure to high levels of air pollution in the urban population (8) .…”

Section: Epidemiology Of Dry Eye Related To Environmental Factorsmentioning

confidence: 83%

“…During acute and chronic phases, specific cell types, inflammatory mediators, and neurotransmitters are involved (78) . Such responses vary depending on the nature and intensity of the stimulus and some mediators have been pointed as major contributors in the process of ocular surface damage related to environmental factors.…”

Section: Epidemiology Of Dry Eye Related To Environmental Factorsmentioning

confidence: 99%

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Is dry eye an environmental disease?

Alves¹,

Novaes²,

Morraye³

et al. 2014

Arquivos Brasileiros De Oftalmologia

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Previous studies have revealed that eye contact with either air pollutants or adverse indoor and/or outdoor environmental conditions can affect tear film composition and ocular surface components. These effects are mediated by selective binding of the environmental agents to ocular surface membrane receptors, leading to activation of pro inflammatory signaling pathways. The aim of the current review was to examine the published evidence associated with environmental factors and ocular surface disease and dry eye. Specifically, the reader will appreciate why it is possible to refer to them as mediators of Environmental Dry Eye Disease (EDED), a singular clinical entity inside DED context, directly caused by pollutants and/ or adverse climatic conditions. The indicators and clinical findings are described along with EDE differential diagnosis in its acute and the chronic phases. Based on strong existing evidence of clinical reports and epidemiological observations regarding DED and environmental factors we conclude that there is a straight cause-and-effect relationship between ambient stresses and DED. International standards and web-based tools are described for monitoring worldwide environmental conditions referring localities and populations susceptible to EDED. This information is beneficial to health providers to pinpoint the individuals and predisposed groups afflicted with DED. Such insights may not only improve the understanding and treatment of DED but also help to identify the contributing factors and lower the frequency and progression of EDED. of DED has been studied and confirmed in animal models of human DED (13)(14)(15) . KeywordsAs indicated, a healthy and pain-free ocular surface depends on identifying and eliminating factors that cause ambient humidity, airflow and purity, and temperature to intolerable levels. Such an undertaking is needed to preserve tear film qualities commensurate with ocular surface health. This is essential to sustain sufficient corneal refractive power, visual acuity, and ocular comfort (5,16,17) . A desiccating environment can lead to increase in tear film evaporation and/or decline in its turn over and clearance. These initial events lead to exposure of the ocular surface to hazardous environmental elements that trigger or exacerbate EDED symptoms. Clinical findings have shown that increased numbers of people are affected by EDED because of exposure to environmental factors ( Figure 2).Our purpose herein is to provide a critical appraisal of the clinical and epidemiological evidence indicating that DED is influenced by environmental factors. Secondly, we delineate EDED as a single clinical entity with a unique set of symptoms and clinical findings different from that of either DED or other diseases, such as Sjögren's syndrome, diabetes mellitus or drug induced, allergic conjunctivitis, toxic or irritative conjunctivitis, and actinic keratitis. Moreover, we will describe standard tools used to monitor environmental conditions and discuss their relevance in EDED ep...

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Section: Epidemiology Of Dry Eye Related To Environmental Factorsmentioning

confidence: 83%

Section: Epidemiology Of Dry Eye Related To Environmental Factorsmentioning

confidence: 99%

Is dry eye an environmental disease?

Alves¹,

Novaes²,

Morraye³

et al. 2014

Arquivos Brasileiros De Oftalmologia

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show abstract

“…TLRs) and induces downstream inflammatory signaling cascade producing proinflammatory mediators to combat the infection [27] . Several groups have shown that TLRs recognize pathogens during ocular infection [26,27] . Recently, others and we have shown that TLR4 is expressed by HCE cells and is responsible for the recognition of Acanthamoeba trophozoites [24,40,41] .…”

Section: Discussionmentioning

confidence: 99%

“…An investigation of the mechanism of the TLR4 signaling cascade that produces cytokines and chemokines discovered that the TLR4 receptor works in a complex of proteins that permit for the identification of its known specific ligand, LPS [26,27] . LPS binding protein (LBP), cluster of differentiation 14 (CD14, a pattern recognition receptor), and myeloid differentiation protein 2 (MD-2) are all expressed in the eye.…”

Section: Research Articlementioning

confidence: 99%

Identification of Acanthamoeba Membrane Protein That is Recognized by TLR4 on Corneal Epithelial Cells

Tripathi

Abdi

Alizadeh

2015

Receptor Clin Invest

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We have shown that Acanthamoeba spp. activate TLR4 on corneal epithelial cells and induce secretion of chemokines. However, the components of Acanthamoeba trophozoites that induce chemokines production remain unknown. We sought to identify the trophozoite molecules that interact with TLR4 on human corneal epithelial (HCE) cells and trigger IL-8 production. Acanthamoeba membrane protein (AcMP) was isolated by homogenization of trophozoites. The supernatants were collected, solubilized, and membrane fractions were separated by centrifugation using Mem-PER TM plus kit. To examine functional activity of AcMP, HCE and TLR4-expressing HEK293 cells were incubated with or without A. castellanii (1×10 5 cells/ml) and AcMP (10, 25, and 50 µg/ml) for 24 hours. AcMP was chromatographed by fast protein liquid chromatography (FPLC) and fractions were pooled into four peaks (AcMP-P1 -AcMP-P4). TLR4-ligand in AcMP-P1 -AcMP-P4 was determined by Western blotting. HEK293 and HCE cells were incubated with or without A. castellanii, lipopolysaccharide (LPS, 10 µg/ml), and AcMP-P1 -AcMP-P4 (20 µg/ml) for 24 hours. qRT-PCR and ELISA were used to examine the ability of AcMP-P1 -AcMP-P4 to stimulate IL-8 production in HEK293 and HCE cells. Inhibition of TLR4 involved preincubating HEK293 and HCE cells for 1 hour with neutralizing TLR4-antibody (10 µg/ml) or with the control antibody (10 µg/ml, goat serum) followed by incubation with or without A. castellanii, LPS, and AcMP-P2 for 24 hours. AcMP induced significant IL-8 production at doses of 10, 25, and 50 µg/ml in HEK293 cells while IL-8 mRNA expression and IL-8 secretion were significantly increased in HCE cells at the dose of 50 µg/ml. Treatments of HEK293 with FPLC chromatographed trophozoites' proteins, AcMP-P1 -AcMP-P4; only AcMP-P2 upregulated significant IL-8 production and mRNA expression. Western blotting of AcMP-P1 -AcMP-P4 showed TLR4-antigen in AcMP-P2 and was recognized an approximate 15-kDa protein band. Anti-TLR4 antibody attenuated IL-8 secretion that is stimulated by AcMP-P2 from HEK293 and HCE cells. These results suggest that A. castellanii trophozoites recognize TLR4 on HCE and HEK293 cells by an approximate 15-kDa molecular mass protein of AcMP and induce IL-8 secretion.

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“…Clinical symptoms are also indication for measuring intraocular pressure. Persistent conjunctival hyperemia or chronic ocular surface inammation [9,10] should especially be paid attention to. The intraocular pressure measurement is based on the principles of uid mechanics [11].…”

Section: Introductionmentioning

confidence: 99%

Reconstruction of Lost Fragments of Signal Received from the Wireless Sensor Measuring Fluid Pressure inside the Eye Ball

2015

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The aim of the paper is to present a technique of reconstructing data received from a wireless sensor for measuring intraocular pressure. The algorithm was developed to automatically regenerate samples lost due to fortuitous events in clinical trials. The test consisted in measuring the pressure within 24 h, during which the intraocular pressure curve were determined. The paper also discusses the structure and the physical basis of sensor operation and shows the advantages resulting from its use.

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Pathways of Corneal and Ocular Surface Inflammation: A Perspective from the Cullen Symposium

Cited by 49 publications

References 3 publications

Is dry eye an environmental disease?

Is dry eye an environmental disease?

Identification of Acanthamoeba Membrane Protein That is Recognized by TLR4 on Corneal Epithelial Cells

Reconstruction of Lost Fragments of Signal Received from the Wireless Sensor Measuring Fluid Pressure inside the Eye Ball

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