scholarly journals Review: The Lacrimal Gland and Its Role in Dry Eye

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Christopher D. Conrady ◽  
Zachary P. Joos ◽  
Bhupendra C. K. Patel
Keyword(s):  
Dry Eye ◽  
Lacrimal Gland ◽  
Ocular Surface ◽  
Tear Film ◽  
Burning Pain ◽  
Layered Coating ◽  
Accessory Glands ◽  
Multiple Components ◽  
Blurry Vision

The human tear film is a 3-layered coating of the surface of the eye and a loss, or reduction, in any layer of this film may result in a syndrome of blurry vision and burning pain of the eyes known as dry eye. The lacrimal gland and accessory glands provide multiple components to the tear film, most notably the aqueous. Dysfunction of these glands results in the loss of aqueous and other products required in ocular surface maintenance and health resulting in dry eye and the potential for significant surface pathology. In this paper, we have reviewed products of the lacrimal gland, diseases known to affect the gland, and historical and emerging dry eye therapies targeting lacrimal gland dysfunction.

scholarly journals Dry eye modifies the thermal and menthol responses in rat corneal primary afferent cool cells

2013 ◽  
Vol 110 (2) ◽  
pp. 495-504 ◽  
Author(s):  
Masayuki Kurose ◽  
Ian D. Meng
Keyword(s):  
Dry Eye ◽  
Lacrimal Gland ◽  
Ocular Surface ◽  
Transient Receptor Potential ◽  
Tear Film ◽  
Receptor Potential ◽  
Peak Frequency ◽  
Painful Condition ◽  
Primary Afferent ◽  
Transient Receptor Potential Melastatin

Dry eye syndrome is a painful condition caused by inadequate or altered tear film on the ocular surface. Primary afferent cool cells innervating the cornea regulate the ocular fluid status by increasing reflex tearing in response to evaporative cooling and hyperosmicity. It has been proposed that activation of corneal cool cells via a transient receptor potential melastatin 8 (TRPM8) channel agonist may represent a potential therapeutic intervention to treat dry eye. This study examined the effect of dry eye on the response properties of corneal cool cells and the ability of the TRPM8 agonist menthol to modify these properties. A unilateral dry eye condition was created in rats by removing the left lacrimal gland. Lacrimal gland removal reduced tears in the dry eye to 35% compared with the contralateral eye and increased the number of spontaneous blinks in the dry eye by over 300%. Extracellular single-unit recordings were performed 8–10 wk following surgery in the trigeminal ganglion of dry eye animals and age-matched controls. Responses of corneal cool cells to cooling were examined after the application of menthol (10 μM–1.0 mM) to the ocular surface. The peak frequency of discharge to cooling was higher and the cooling threshold was warmer in dry eye animals compared with controls. The dry condition also altered the neuronal sensitivity to menthol, causing desensitization to cold-evoked responses at concentrations that produced facilitation in control animals. The menthol-induced desensitization of corneal cool cells would likely result in reduced tearing, a deleterious effect in individuals with dry eye.

scholarly journals Therapeutical approach to dry eye syndrome

2010 ◽  
Vol 63 (11-12) ◽  
pp. 793-800 ◽  
Author(s):  
Gordana Stankovic-Babic ◽  
Gordana Zlatanovic ◽  
Jasmina Djordjevic-Jocic ◽  
Sonja Cekic ◽  
Milena Vujanovic
Keyword(s):  
Dry Eye ◽  
Lacrimal Gland ◽  
Ocular Surface ◽  
Cell Damage ◽  
Tear Film ◽  
Dry Eye Disease ◽  
Eye Disease ◽  
Inflammatory Disorder ◽  
Therapeutic Modalities ◽  
Third Line

Introduction. Dry eye disease or dysfunctional tear syndrome is among the most frequently established diagnoses in ophthalmology. It can be defined as a disorder of the tear film resulting in changes in the ocular surface. Mechanisms in development of dry eye disease. There are many factors causing dry eye and they can be related to deficiency in any of the components of the tear film. It has been suggested that dry eye is an inflammatory disorder that affects the ocular surface and lacrimal gland. Inflammation is the most important mechanism of corneal and conjunctival cell damage, which is responsible for the symptoms and signs of ocular surface pathology. Hormonal imbalance (particularly androgens), neural dysfunction, increased levels of pro-inflammatory cytokines and loss of immune homeostasis of the lacrimal gland and ocular surface could be possible mechanisms in the pathogenesis of dry eye disease. Discussion. The aim of this paper was to review the advances in the pathogenesis and management of the dry eye disease. The appropriate dry eye treatment presupposes knowledge of all existing pharmacologic and non-pharmacologic therapeutic modalities. The mainstay of therapy is still artificial tears, with anti-inflammatory therapy and punctual occlusion therapy as second and third line therapies.

scholarly journals Tear Proteomics Study of Dry Eye Disease: Which Eye Do You Adopt as the Representative Eye for the Study?

2021 ◽  
Vol 22 (1) ◽  
pp. 422
Author(s):  
Ming-Tse Kuo ◽  
Po-Chiung Fang ◽  
Shu-Fang Kuo ◽  
Alexander Chen ◽  
Yu-Ting Huang
Keyword(s):  
Dry Eye ◽  
Ocular Surface ◽  
Tear Film ◽  
Dry Eye Disease ◽  
Eye Disease ◽  
Mechanistic Studies ◽  
Clinical Tests ◽  
Tear Proteins ◽  
Proteomic Data ◽  
Surface Performance

Most studies about dry eye disease (DED) chose unilateral eye for investigation and drew conclusions based on monocular results, whereas most studies involving tear proteomics were based on the results of pooling tears from a group of DED patients. Patients with DED were consecutively enrolled for binocular clinical tests, tear biochemical markers of DED, and tear proteome. We found that bilateral eyes of DED patients may have similar but different ocular surface performance and tear proteome. Most ocular surface homeostatic markers and tear biomarkers were not significantly different in the bilateral eyes of DED subjects, and most clinical parameters and tear biomarkers were correlated significantly between bilateral eyes. However, discrepant binocular presentation in the markers of ocular surface homeostasis and the associations with tear proteins suggested that one eye’s performance cannot represent that of the other eye or both eyes. Therefore, in studies for elucidating tear film homeostasis of DED, we may lose some important messages hidden in the fellow eye if we collected clinical and proteomic data only from a unilateral eye. For mechanistic studies, it is recommended that researchers collect tear samples from the eye with more severe DED under sensitive criteria for identifying the more severe eye and evaluating the tear biochemical and proteomic markers with binocular concordance drawn in prior binocular studies.

scholarly journals Apigenin ameliorates ocular surface lesions in a rat model of dry eye disease

2019 ◽  
Vol 17 ◽  
pp. 205873921881868
Author(s):  
Limei Liu ◽  
Dongdong Wei ◽  
Hongkun Xu ◽  
Changhui Liu
Keyword(s):  
Dry Eye ◽  
Ocular Surface ◽  
Histopathological Examination ◽  
Tear Film ◽  
Interleukin 10 ◽  
Dry Eye Disease ◽  
Eye Disease ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Necrosis Factor Alpha

To study the effects of apigenin on dry eye disease (DED) in rats. Rats were divided into six groups: (I) normal control group, (II) DED control group, (III) vehicle control group, (IV) DED + apigenin 10 mg/kg, (V) DED + apigenin 20 mg/kg, and (VI) DED + apigenin 50 mg/kg. Schirmer test, tear film break-up time (BUT), and corneal fluorescein staining were used to evaluate the effects of apigenin on the ocular surface. The related inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Histopathological examination and inflammatory index were also performed. The results showed that administration of apigenin was shown a significant effect on the recovery of ocular surface function. Compared to the control group, apigenin treatment in DED rats significantly decreased the level of the tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6); however, the interleukin-10 (IL-10) level was increased. Histopathological examination further verified the anti-inflammatory effects of apigenin on DED rats. The results demonstrated that apigenin could protect DED rats via inhibition of inflammation, suggesting that it may have potential as a therapy for DED.

scholarly journals In Vivo Anti-Inflammation Potential of Aster koraiensis Extract for Dry Eye Syndrome by the Protection of Ocular Surface

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3245
Author(s):  
Sung-Chul Hong ◽  
Jung-Heun Ha ◽  
Jennifer K. Lee ◽  
Sang Hoon Jung ◽  
Jin-Chul Kim
Keyword(s):  
Animal Model ◽  
Er Stress ◽  
Dry Eye ◽  
Lacrimal Gland ◽  
Ocular Surface ◽  
Inflammatory Responses ◽  
Dry Eye Syndrome ◽  
Inhibitory Effects ◽  
Food Material

Dry eye syndrome (DES) is a corneal disease often characterized by an irritating, itching feeling in the eyes and light sensitivity. Inflammation and endoplasmic reticulum (ER) stress may play a crucial role in the pathogenesis of DES, although the underlying mechanism remains elusive. Aster koraiensis has been used traditionally as an edible herb in Korea. It has been reported to have wound-healing and inhibitory effects against insulin resistance and inflammation. Here, we examined the inhibitory effects of inflammation and ER stress by A. koraiensis extract (AKE) in animal model and human retinal pigmented epithelial (ARPE-19) cells. Oral administration of AKE mitigated DE symptoms, including reduced corneal epithelial thickness, increased the gap between lacrimal gland tissues in experimental animals and decreased tear production. It also inhibited inflammatory responses in the corneal epithelium and lacrimal gland. Consequently, the activation of NF-κB was attenuated by the suppression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). Moreover, AKE treatment ameliorated TNF-α-inducible ocular inflammation and thapsigargin (Tg)-inducible ER stress in animal model and human retinal pigmented epithelial (ARPE-19) cells. These results prove that AKE prevents detrimental functional and histological remodeling on the ocular surface and in the lacrimal gland through inhibition of inflammation and ER stress, suggesting its potential as functional food material for improvement of DES.

scholarly journals Role of ion channels in the functional response of conjunctival goblet cells to dry eye

2018 ◽  
Vol 315 (2) ◽  
pp. C236-C246 ◽  
Author(s):  
Donald G. Puro
Keyword(s):  
Ion Channels ◽  
Dry Eye ◽  
Ocular Surface ◽  
Adaptive Response ◽  
Tear Film ◽  
Goblet Cells ◽  
Cation Conductance ◽  
Conjunctival Goblet Cells

Optimal vision requires an ocular surface with a stable tear film whose many critical tasks include providing >70% of the eye’s refractive power. However, for millions, tear film instability produces uncomfortable sight-impairing dry eye. Despite the multitude of etiologies for dry eye, a universal hallmark is hyperosmolarity of the tear film. Presently, knowledge of how the ocular surface responds to hyperosmolarity remains incomplete with little understood about the role of ion channels. This bioelectric analysis focused on conjunctival goblet cells whose release of tear-stabilizing mucin is a key adaptive response to dry eye. In freshly excised rat conjunctiva, perforated-patch recordings demonstrated that a ≥10% rise in osmolarity triggers goblet cells to rapidly generate a ~15-mV hyperpolarization due to the oxidant-dependent activation of ATP-sensitive K+ (KATP) channels. High-resolution membrane capacitance measurements used to monitor exocytosis revealed that this hyperpolarization results in an approximately fourfold boost in exocytotic activity evoked by cholinergic input, which in vivo occurs via a neural reflex and depends chiefly on calcium influxing down its electro-gradient. We discovered that this adaptive response is transient. During 30–80 min of hyperosmolarity, development of a depolarizing nonspecific cation conductance fully counterbalances the KATP-driven hyperpolarization and thereby eliminates the exocytotic boost. We conclude that hyperosmotic-induced hyperpolarization is a previously unappreciated mechanism by which goblet cells respond to transient ocular dryness. Loss of this voltage increase during long-term dryness/hyperosmolarity may account for the clinical conundrum that goblet cells in chronically dry eyes can remain filled with mucin even though the tear film is hyperosmotic and mucin-deficient.

scholarly journals Diagnostic Procedures and Management of Dry Eye

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Snježana Kaštelan ◽  
Martina Tomić ◽  
Jasminka Salopek-Rabatić ◽  
Branko Novak
Keyword(s):  
Dry Eye ◽  
Ocular Surface ◽  
Tear Film ◽  
Diagnostic Procedures ◽  
Female Gender ◽  
Dry Eye Disease ◽  
Eye Disease ◽  
Systematic Classification ◽  
Contact Lens Wear ◽  
Potential Damage

Dry eye disease or dysfunctional tear syndrome is among the most frequent diagnoses in ophthalmology. It is a multifactorial disease of the ocular surface and tear film which results in ocular discomfort, visual disturbances, and tear instability with potential damage to the cornea and conjunctiva. Risk factors for dry eye syndrome include age, sex (female gender), race, contact lens wear, environment with low humidity, systemic medications, and autoimmune disorders. The aim of this paper is to present the systematic classification, epidemiology, diagnostic procedures, and advances in the management of dry eye disease. The recent improvements in comprehending the underlying etiologic factors will inevitably improve future classifications and diagnostic abilities leading to more effective therapeutic options. Treatment of this highly prevalent condition can drastically improve the quality of life of individuals and prevent damage to the ocular surface.

Expression of CCR5 and Its Ligands CCL3, -4, and -5 in the Tear Film and Ocular Surface of Patients with Dry Eye Disease

2011 ◽  
Vol 37 (1) ◽  
pp. 12-17 ◽  
Author(s):  
Won Choi ◽  
Zhengri Li ◽  
Han-Jin Oh ◽  
Seong-Kyu Im ◽  
Seung-Hyun Lee ◽  
...  
Keyword(s):  
Dry Eye ◽  
Ocular Surface ◽  
Tear Film ◽  
Dry Eye Disease ◽  
Eye Disease
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