Role of ocular surface neurobiology in neuronal-mediated inflammation in dry eye disease

Asiedu, Kofi

doi:10.1016/j.npep.2022.102266

Cited by 13 publications

(35 citation statements)

References 243 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have shown that the neurosensory abnormalities in dry eye are due to abnormal expression of ion channels and their functional abnormalities, hypersensitivity or injury to corneal nociceptors, and neuroinflammatory cascade via secretion of neuropeptides and other neuromediators. 7,8,34 In laser-assisted in situ keratomileusis (LASIK), corneal nerve loss is associated with the severity of dry eye symptoms and clinical signs 35 ; however, corneal nerve loss in LASIK is quite different from type 2 diabetes mellitus. In LASIK, the corneal nerve loss is acute, and it is accompanied by an increased level of tear neuropeptides and neurotrophins, which instigate neuroinflammatory pathways; however, in type 2 diabetes mellitus, there is gradual loss of corneal nerve fibers, and no difference in tear neuropeptide level is noted between type 2 diabetes mellitus and healthy controls.…”

Section: Discussionmentioning

confidence: 99%

“…These findings suggest that other mechanisms may underlie the pathogenesis of dry eye disease in these two groups aside from corneal nerve loss. Studies have shown that the neurosensory abnormalities in dry eye are due to abnormal expression of ion channels and their functional abnormalities, hypersensitivity or injury to corneal nociceptors, and neuroinflammatory cascade via secretion of neuropeptides and other neuromediators 7,8,34 …”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Impact of Peripheral and Corneal Neuropathy on Markers of Ocular Surface Discomfort in Diabetic Chronic Kidney Disease

Asiedu¹,

Dhanapalaratnam

Krishnan

et al. 2022

Optom Vis Sci

Self Cite

View full text Add to dashboard Cite

SIGNIFICANCEThere is a reduction in corneal nerve fiber density and length in type 2 diabetes mellitus with chronic kidney disease compared with type 2 diabetes mellitus alone; however, this difference does not result in worse ocular surface discomfort or dry eye disease.PURPOSEThis study aimed to determine the clinical impact of corneal nerve loss on ocular surface discomfort and markers of ocular surface homeostasis in people with type 2 diabetes mellitus without chronic kidney disease (T2DM–no CKD) and those with type 2 diabetes mellitus with concurrent chronic kidney disease (T2DM-CKD).METHODSParticipants were classified based on estimated glomerular filtration rates into two groups: T2DM-CKD (n = 27) and T2DM–no CKD (n = 28).RESULTSThere was a significant difference between the T2DM-CKD and T2DM–no CKD groups in corneal nerve fiber density (14.9 ± 8.6 and 21.1 ± 7.1 no./mm2, respectively; P = .005) and corneal nerve fiber length (10.0 ± 4.6 and 12.3 ± 3.7 mm/mm2, respectively; P = .04). Fluorescein tear breakup time was significantly reduced in T2DM-CKD compared with T2DM–no CKD (8.1 ± 4.4 and 10.7 ± 3.8 seconds, respectively; P = .01), whereas ocular surface staining was not significantly different (3.5 ± 1.7 and 2.7 ± 2.3 scores, respectively;P = .12). In terms of ocular surface discomfort, there were no significant differences in the ocular discomfort score scores (12.5 ± 11.1 and 13.6 ± 12.1, respectively; P = .81) and Ocular Pain Assessment Survey scores (3.3 ± 5.4 and 4.3 ± 6.1, respectively; P = .37) between the T2DM-CKD and T2DM–no CKD.CONCLUSIONSThe current study demonstrated that corneal nerve loss is greater in T2DM-CKD than in T2DM–no CKD. However, these changes do not impact ocular surface discomfort or markers of ocular surface homeostasis.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Impact of Peripheral and Corneal Neuropathy on Markers of Ocular Surface Discomfort in Diabetic Chronic Kidney Disease

Asiedu¹,

Dhanapalaratnam

Krishnan

et al. 2022

Optom Vis Sci

Self Cite

View full text Add to dashboard Cite

show abstract

“…The transient receptor potential (TRP) family is thought to transduce environmental and endogenous stimuli to electrophysiological signals. TRPV1 is a well-characterised channel expressed by a subset of peripheral sensory neurons, and canonically mediates inflammatory and neuropathic pain (163). TRPV1 sensitization can be induced by capsaicin.…”

Section: Neural Ion Channels Changesmentioning

confidence: 99%

Mechanistic investigations of diabetic ocular surface diseases

et al. 2022

View full text Add to dashboard Cite

With the global prevalence of diabetes mellitus over recent decades, more patients suffered from various diabetic complications, including diabetic ocular surface diseases that may seriously affect the quality of life and even vision sight. The major diabetic ocular surface diseases include diabetic keratopathy and dry eye. Diabetic keratopathy is characterized with the delayed corneal epithelial wound healing, reduced corneal nerve density, decreased corneal sensation and feeling of burning or dryness. Diabetic dry eye is manifested as the reduction of tear secretion accompanied with the ocular discomfort. The early clinical symptoms include dry eye and corneal nerve degeneration, suggesting the early diagnosis should be focused on the examination of confocal microscopy and dry eye symptoms. The pathogenesis of diabetic keratopathy involves the accumulation of advanced glycation end-products, impaired neurotrophic innervations and limbal stem cell function, and dysregulated growth factor signaling, and inflammation alterations. Diabetic dry eye may be associated with the abnormal mitochondrial metabolism of lacrimal gland caused by the overactivation of sympathetic nervous system. Considering the important roles of the dense innervations in the homeostatic maintenance of cornea and lacrimal gland, further studies on the neuroepithelial and neuroimmune interactions will reveal the predominant pathogenic mechanisms and develop the targeting intervention strategies of diabetic ocular surface complications.

show abstract

“…Recent studies have revealed the role of central sensitization and neuroinflammation in the development of corneal neuropathic pain of DED. 4 , 5 , 6 The abnormal sensory message transmitted to the central nervous system (CNS) may affect the excitability of sensory neurons of the associated brain regions and induce corneal neuropathic pain symptoms. However, the cellular and molecular mechanisms of the brain areas related to corneal neuropathic pain need further investigation.…”

Section: Introductionmentioning

confidence: 99%

Alteration of neural activity and neuroinflammatory factors in the insular cortex of mice with corneal neuropathic pain

Zhang

et al. 2023

Genes Brain and Behavior

View full text Add to dashboard Cite

Dry eye disease (DED) affects nearly 55% of people worldwide; several studies have proposed that central sensitization and neuroinflammation may contribute to the developing corneal neuropathic pain of DED, while the underlying mechanisms of this contribution remain to be investigated. Excision of extra orbital lacrimal glands established the dry eye model. Corneal hypersensitivity was examined through chemical and mechanical stimulation, and open field test measured the anxiety levels. Restingstate fMRI is a method of functional magnetic resonance imaging (rs‐fMRI) was performed for anatomical involvement of the brain regions. The amplitude of low‐frequency fluctuation (ALFF) determined brain activity. Immunofluorescence testing and Quantitative real‐time polymerase chain reaction were also performed to further validate the findings. Compared with the Sham group, ALFF signals in the supplemental somatosensory area, secondary auditory cortex, agranular insular cortex, temporal association areas, and ectorhinal cortex brain areas were increased in the dry eye group. This change of ALFF in the insular cortex was linked with the increment in corneal hypersensitivity (p < 0.01), c‐Fos (p < 0.001), brain‐derived neurotrophic factor (p < 0.01), TNF‐α, IL‐6, and IL‐1β (p < 0.05). In contrast, IL‐10 levels (p < 0.05) decreased in the dry eye group. DED‐induced corneal hypersensitivity and upregulation of inflammatory cytokines could be blocked by insular cortex injection of Tyrosine Kinase receptor B agonist cyclotraxin‐B (p < 0.01) without affecting anxiety levels. Our study reveals that the functional activity of the brain associated with corneal neuropathic pain and neuroinflammation in the insular cortex might contribute to dry eye‐related corneal neuropathic pain.

show abstract

Role of ocular surface neurobiology in neuronal-mediated inflammation in dry eye disease

Cited by 13 publications

References 243 publications

Impact of Peripheral and Corneal Neuropathy on Markers of Ocular Surface Discomfort in Diabetic Chronic Kidney Disease

Impact of Peripheral and Corneal Neuropathy on Markers of Ocular Surface Discomfort in Diabetic Chronic Kidney Disease

Mechanistic investigations of diabetic ocular surface diseases

Alteration of neural activity and neuroinflammatory factors in the insular cortex of mice with corneal neuropathic pain

Contact Info

Product

Resources

About