Various proinflammatory cytokines that may cause cellular destruction, including interleukin (IL)-1, IL-6, IL-8, transforming growth factor beta (TGF-beta), tumor necrosis factor alpha (TNF-alpha), and chemokine ligand 5 (CCL5 or RANTES), are typically altered in patients with DED. IL-1 beta and TNF-alpha, which are present in the tears primarily of patients with inflammatory dry eye, cause the release of opioids that bind to opioid receptors on neural membranes and inhibit neurotransmitter release. In addition to inhibiting neural function, inflammatory cytokines may also convert androgens into estrogens, resulting in meibomian gland dysfunction. An increased rate of apoptosis also is seen in conjunctival and lacrimal acinar cells.
Proinflammatory neurotransmitters, such as substance P and CGRP, are released, and these substances recruit and activate local lymphocytes. Studies suggest that dry eye severity is directly correlated with nerve growth factor levels and inversely correlated with CGRP and neuropeptide Y tear levels.
Learn more about the pathophysiology of DED.
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Cite this: Christina R. Prescott. Fast Five Quiz: Dry Eye Disease (Keratoconjunctivitis Sicca) Etiology and Pathophysiology - Medscape - Nov 10, 2022.