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2021 OMIG Abstract
Intraocular Inflammasome Activation in Corneal Graft Failure
Andres Serrano1,2, Angela Gomez-Bedoya1,2, Arianna Tovar1,2, Patrice J. Persad1, Guillermo Amescua1, Ellen Koo1, Florence Cabot1, Roey Hadad3, Juan Pablo de Rivero Vaccari3, Alfonso L. Sabater1,2
1Bascom Palmer Eye Institute, Miami,Florida; 2Cornea and Ocular Surface Regenerative Medicine Center, Miami, Florida; 3The Miami Project to Cure Paralysis, University of Miami, Miami, Florida
Purpose: High intraocular levels of proinflammatory cytokines have been associated with primary graft failure and endothelial cell loss after corneal transplant. However, it is unknown which mechanism is involved in this interaction. Some proteins (apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), caspase-1, interleukin (IL)-18 and IL-1β) have been identified as part of the inflammasome signaling pathway, a key mechanism of the innate immune response involved in inflammation and cell death. In the present study, we measured the intraocular levels of inflammasome signaling proteins in patients with corneal graft failure (CGF) to assess whether this pathway contributes to graft failure, and whether these proteins correlate with clinical parameters such as central corneal thickness (CCT) and ocular surface inflammation.
Methods: Aqueous humor (AqH) samples from 16 patients were analyzed. Samples were collected at the beginning of surgery from patients with CGF (n=7) who underwent corneal transplantation, and healthy controls who underwent cataract surgery (n=9). Inflammasome involvement was assessed by measuring the presence of the inflammasome signaling proteins (ASC, caspase-1, IL-18, and IL-1β) in AqH samples via Simple Plex technology (Protein Simple). Additionally, we studied the association between inflammasome signaling protein expression and clinical parameters (CCT measured by ultrasound pachymetry, and ocular surface inflammation measured by InflammaDry® tear immunoassay) among the subjects.
Results: The presence of inflammasome-mediated cell death markers differed significantly across the AqH of patients with CGF (7/7; 100%) compared with the control group (0/9; 0%) (Fisher’s exact test p=< 0.0001). Regarding clinical measurements, subjects with detectable protein levels in the AqH presented significantly higher CCTs than subjects with undetectable markers [Mann-Whitney U, or Wilcoxon test p=0.001]. The InflammaDry® test did not show significant differences among patients with detectable and non-detectable AqH markers (Fisher’s exact test p=0.14).
Conclusions: Detectable levels of inflammasome-mediated cell death markers in the AqH of patients with CGF suggest that the inflammasome may play an important role in the pathogenesis of this condition and should be further studied for therapeutic purposes. Moreover, this could aid to a better management of patients with transplanted corneas in combination with parameters used during standard clinic visits.
Disclosure: P, C (JPdRV)
Support: This research was supported by the Florida Lions Eye Bank, the Beauty of Sight Foundation (Dr. Sabater), NIH Center Core Grant P30EY014801 and Research to Prevent Blindness Unrestricted Grant.
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