Association of increased levels of plasma tumor necrosis factor alpha with primary open-angle glaucoma

Abstract

PurposeRetinal ganglion cell (RGC) death is a key feature of glaucoma. Elevated levels of tumor necrosis factor alpha (TNF-α), a pro-inflammatory cytokine, can induce RGC apoptosis and play a critical role in glaucomatous neurodegeneration. Based on the possible role of inflammation and oxidative stress in the pathogenesis of primary open-angle glaucoma (POAG), we investigated the association between plasma levels of TNF-α and POAG or its clinical indices in comparison to non-glaucomatous controls.Patients and methodsIn a case–control retrospective cohort of 51 POAG cases and 88 controls, plasma TNF-α levels were measured using an enzyme-linked immunosorbent assay (ELISA). The assay was performed in duplicates on an automated ELISA analyzer.ResultsMean TNF-α level was significantly elevated in POAG cases (1.88 ± 2.17 pg/mL) than the controls (0.93 ± 1.49 pg/mL; p = 0.003). The overall dose–response trend was significant (χ2 = 6.12, df = 2; p = 0.047). No statistical difference was seen in age, gender and systemic disease distribution. A modest negative and significant correlation was seen between TNF-α level and number of antiglaucoma medications, an important clinical index of POAG severity. Moreover, logistic regression analysis showed that the risk of POAG was most significantly affected by TNF-α level and not by age and sex.ConclusionHigh systemic level of an inflammatory cytokine, TNF-α, is associated with POAG; however, its possible use as a biomarker for early glaucoma diagnosis and/or disease severity needs further investigation.

Obstructive sleep apnea as a risk factor for primary open angle glaucoma and ocular hypertension in a monocentric pilot study

“…Other authors have speculated that an elevated neutrophil-to-lymphocyte ratio and the systemic immune inflammation index might serve as predictors for POAG [ 24 ]. Kondkar et al found high systemic level of the inflammatory cytokine TNF-α in their study of 51 POAG patients, compared to 88 controls [ 25 ]. Nonetheless, the mechanisms linking increased intraocular pressure to increased systemic inflammation have not been sufficiently elucidated so far.…”

A comprehensive map of disease networks and molecular drug discoveries for glaucoma

“…Propranolol derivatives have similar pharmacological effects to those of currently used glaucoma drugs and have potential for drug development as www.nature.com/scientificreports www.nature.com/scientificreports/ antiglaucoma agents. In the DGIdb, celecoxib, paclitaxel, and cyclosporine appeared frequently, suggesting that antineoplastic drugs may represent a new direction for glaucoma drug screening 57 .…”

Profile of cytokines in aqueous humor and trabecular meshwork cell culture in patients with pseudoexfoliation glaucoma

“…Это взаимодействие осуществляется посредством выработки различных цитокинов, хемокинов, нейротрофических факторов и других сигнальных молекул, которые участвуют в синтезе, деградации и модификации различных компонентов ЭЦМ трабекулярной сети [6]. В литературе приведены данные исследований, в которых оценивались концентрации цитокинов в биологических жидкостях и тканях у больных с различными формами глаукомы: сыворотке крови [23, 24,25,31], водянистой влаге (ВВ) [8,9,31,36], слезе [9,17], лизате клеток трабекулярной сети [27]. ПЭ синдром является фактором риска развития ПЭ глаукомы и представляет собой ассоциированное с возрастом системное нарушение фибриллогенеза, которое возникает в результате повышенного образования и неправильной сборки компонентов эластиновых микрофибрилл, что приводит к отложению в различных тканях аномального фибриллярного материала [11].…”