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FEATURED ORIGINAL ARTICLE
Year : 2017  |  Volume : 65  |  Issue : 11  |  Page : 1105-1108

Altered tear inflammatory profile in Indian keratoconus patients - The 2015 Col Rangachari Award paper


1 Department of Cornea and Refractive Surgery, Narayana Nethralaya Eye Institute, Bengaluru, Karnataka, India
2 GROW Research Lab, Narayana Nethralaya Foundation, Bengaluru, Karnataka, India

Correspondence Address:
Chaitra Jayadev
Department of Ophthalmology, Narayana Nethralaya Eye Institute, 121/C, Chord Road, 1st R Block, Rajaji Nagar, Bengaluru - 560 010, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijo.IJO_233_17

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Purpose: Conventionally, keratoconus (KC) has been considered a noninflammatory corneal ectatic disorder. Recent evidence suggests a possible role of inflammation in the pathogenesis of KC. Hence, we analyzed the levels of inflammatory factors in the tear fluid of Indian KC patients. Methods: Tear fluid samples were collected from age- and sex-matched healthy controls and KC patients (with different grades). The levels of the inflammatory factors in tears were analyzed using cytometric bead array (Human Soluble Protein Flex Set System, BD Biosciences) for levels of interleukin-1α (IL-1α), IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-9, IL-10, IL-12p70, IL-23p40, IL-13, IL-17A, IL-17F, IL-21, interferon-α (IFNα), IFNγ, tumor necrosis factor-α, CCL2/monocyte chemotactic protein-1, CCL4/macrophage inflammatory protein-1β (MIP-1β), MIP-1α, CCL5/RANTES, CXCL10/IP10, ICAM1, CD62E, vascular endothelial growth factor and transforming growth factor β. Results: An increase in Kmax and Kmean, and a decrease in central corneal thickness was observed with increasing grades of KC. Tear analysis showed that most of the tear soluble factors, including cytokines, chemokines, growth factors and cell adhesion molecules were significantly elevated in the KC patients compared to the controls. Conclusion: Our findings suggest that inflammatory factors associated with KC may play a role in its pathogenesis. This opens the potential to explore anti-inflammatory strategies to either halt or delay the progression of KC.


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