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2021 OMIG Abstract
Caspase-1 As A Biomarker of Ocular Surface Damage
Arianna Tovar1,2, Angela Gomez1,2, Andres Serrano1,2, Maricarmen Perez Blanco1, Anat Galor1,2,
Swarup S. Swaminathan1, Juan Pablo de Rivero Vaccari3, Alfonso L. Sabater1,2
1Department of Ophthalmology, Bascom Palmer Eye Institute, Miami, Florida; 2Cornea and Ocular Surface Regenerative Medicine Center, Miami, Florida; 3Department of Neurological Surgery and The Miami Project to Cure Paralysis,
University of Miami Miller School of Medicine, Miami, Florida
Purpose: Inflammation is a key component in the ocular surface damage associated with dry eye disease (DED). The nod-like receptor protein-3 (NLRP3) inflammasome pathway is an inflammation-induced programmed cell death, in which caspase-1 mediates the activation of interleukins (IL)-18 and IL-1B, and cleaves Gasdermin-D, a protein that creates membrane pores, resulting in cell rupture and release of these pro-inflammatory interleukins. This pathway creates a perpetuate cycle of inflammation that has previously been described to be active in the ocular surface of patients with DED, and that available DED anti-inflammatory therapies have not been able to break.
Our purpose was to examine the potential of caspase-1 as a biomarker of ocular surface damage.
Methods: The ocular surface of 113 eyes (64 subjects) were analyzed, comprised of 20 control eyes, 61 eyes with dry eye disease (DED), and 32 eyes from individuals on topical glaucoma medications. All individuals completed a medical history form, self-responded the ocular surface disease index (OSDI) questionnaire, and underwent an ocular surface assessment: bulbar redness, tear break-up time (TBUT), corneal staining, conjunctival staining, and Schirmer’s tests. Protein levels of caspase-1 were determined with the use of an enzyme-linked immunosorbent assay from Schirmer strip samples. Capsase-1 levels were compared among individuals with signs of ocular surface damage among cases and controls. Secondary correlational analyses were conducted to examine relationships between caspase-1 levels and ocular symptoms and signs. Finally, area under the curve (AUC) analyses were performed to examine relationships between caspase-1 and corneal staining >3 points in the National Eye Institute (NEI) grading scale.
Results: The mean age of the study population was 58±18 years old and 70% were female. Tear samples from individuals with ocular surface damage had higher caspase-1 levels than the control group (DED: p=0.05, Glaucoma: p=0.01). Caspase-1 levels showed a positive correlation with corneal staining (r=0.31, p=0.001) and eye redness (r=0.39, p=0.004) and a negative correlation with Schirmer’s (r=-0.46, p<0.0001) and TBUT (r=-0.33, p=0.0006). It did not show correlation with OSDI scores. A cutoff point of caspase-1=82.85pg/mL showed a high sensitivity (73%) and AUC of 0.7 (p=0.0002, confidence interval: 0.62 to 0.81, SEM: 0.05) for the detection of corneal staining >3 points.
Conclusions: Caspase-1 levels are higher in the tears of individuals with corneal staining >3, pointing at its potential to be used as a biomarker and/or therapeutic target of ocular surface damage.
Disclosure: P, N
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