Lacrimal Gland, Ocular Surface, and Dry Eye

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.

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Review: The Lacrimal Gland and Its Role in Dry Eye

Journal of Ophthalmology ◽

10.1155/2016/7542929 ◽

2016 ◽

Vol 2016 ◽

pp. 1-11 ◽

Cited By ~ 37

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.

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A Ligation of the Lacrimal Excretory Duct in Mouse Induces Lacrimal Gland Inflammation with Proliferative Cells

Stem Cells International ◽

10.1155/2017/4923426 ◽

2017 ◽

Vol 2017 ◽

pp. 1-9 ◽

Cited By ~ 5

Author(s):

Ying Liu ◽

Masatoshi Hirayama ◽

Tetsuya Kawakita ◽

Kazuo Tsubota

Keyword(s):

Dry Eye ◽

Lacrimal Gland ◽

Ocular Surface ◽

Tissue Injury ◽

Dry Eye Disease ◽

Excretory Duct ◽

Eye Disease ◽

Injury Model ◽

Duct Ligation ◽

Number Of Patients

The lacrimal gland secretes tear fluids to ocular surface, which plays an indispensable role in maintaining the health of the ocular epithelia and protecting the ocular surface from the external environment. The dysfunction of the lacrimal glands causes dry eye disease due to a reduction in tear volume. The dry eye disease is becoming a popular public disease, for the number of patients is increasing, who have subjective symptom and loss of vision, which affect the quality of life. Inflammatory change in the damaged lacrimal gland has been reported; however, a major challenge is to establish a simple animal model to observe the changes. Here, we demonstrated an injury model by ligating the main excretory duct of the lacrimal gland, which is a simple and stable way to clearly understand the mechanism of lacrimal gland inflammation. We observed the process of injury and proliferation of the lacrimal gland and detected a population of lacrimal gland epithelial cells with proliferation potential which were also nestin-positive cells following duct ligation. This study successfully established an injury model to observe the tissue injury process of the lacrimal gland, and this model will be useful for analysis of the inflammation and proliferation mechanism in the future.

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Time course of ocular surface and lacrimal gland changes in a new scopolamine-induced dry eye model

Graefe s Archive for Clinical and Experimental Ophthalmology ◽

10.1007/s00417-008-0784-9 ◽

2008 ◽

Vol 246 (6) ◽

pp. 857-867 ◽

Cited By ~ 23

Author(s):

Sabrina Viau ◽

Marie-Annick Maire ◽

Bruno Pasquis ◽

Stéphane Grégoire ◽

Cynthia Fourgeux ◽

...

Keyword(s):

Dry Eye ◽

Lacrimal Gland ◽

Ocular Surface ◽

Time Course ◽

Eye Model

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Isolated bilateral congenital lacrimal gland agenesis presenting as dry eye in childhood: a rare entity

Asian Journal of Ophthalmology ◽

10.35119/asjoo.v17i1.459 ◽

2020 ◽

Vol 17 (1) ◽

pp. 74-77

Author(s):

Anitha Venugopal ◽

Sowmya Peri ◽

Ravi Chandra ◽

Meenakshi Ravindran ◽

Rengappa Ramakrishnan

Keyword(s):

Salivary Glands ◽

Dry Eye ◽

Lacrimal Gland ◽

Ocular Surface ◽

Vitamin Supplementation ◽

Bulbar Conjunctiva ◽

Eye Drops ◽

Rare Entity ◽

Permanent Occlusion ◽

Functional Vision

We report the case of a 1-year-old child who presented with complaints of redness and defective vision since birth. The child had no systemic abnormalities. On examination, complete keratinization of the bulbar conjunctiva and cornea was noted with dry, lustreless and irregular surface. Corneal sensation was intact. Orbital MRI revealed bilateral agenesis of the lacrimal gland with normal salivary glands. The child was given vitamin supplementation, cyclosporine eye drops along with lubricants and tape tarsorrhaphy in the night. Permanent occlusion of both the lower puncta was done. There was decreased ocular surface congestion, with frequent wetting of the ocular surface, which continued in the months to follow. We present a case of isolated bilateral lacrimal gland agenesis with normal salivary glands, a rare cause of dry eye in children. An early diagnosis and conservative management can help in maintaining functional vision in such cases.

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Neutralization of Ocular Surface TNF-α Reduces Ocular Surface and Lacrimal Gland Inflammation Induced by In Vivo Dry Eye

Investigative Opthalmology & Visual Science ◽

10.1167/iovs.12-11515 ◽

2013 ◽

Vol 54 (12) ◽

pp. 7557 ◽

Cited By ~ 27

Author(s):

Yong Woo Ji ◽

Yu Jeong Byun ◽

Wungrak Choi ◽

Eunae Jeong ◽

Jin Sun Kim ◽

...

Keyword(s):

Dry Eye ◽

Lacrimal Gland ◽

Ocular Surface ◽

Tnf Α

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

Journal of Neurophysiology ◽

10.1152/jn.00222.2013 ◽

2013 ◽

Vol 110 (2) ◽

pp. 495-504 ◽

Cited By ~ 39

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.

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Therapeutical approach to dry eye syndrome

Medicinski pregled ◽

10.2298/mpns1012793s ◽

2010 ◽

Vol 63 (11-12) ◽

pp. 793-800 ◽

Cited By ~ 4

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.

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The Protective Effect of Polygonum cuspidatum (PCE) Aqueous Extract in a Dry Eye Model

Nutrients ◽

10.3390/nu10101550 ◽

2018 ◽

Vol 10 (10) ◽

pp. 1550 ◽

Cited By ~ 7

Author(s):

Bongkyun Park ◽

Ik Lee ◽

Soo-Wang Hyun ◽

Kyuhyung Jo ◽

Tae Lee ◽

...

Keyword(s):

Inflammatory Cytokines ◽

Aqueous Extract ◽

Dry Eye ◽

Lacrimal Gland ◽

Ocular Surface ◽

Corneal Epithelial Cell ◽

Heme Oxygenase 1 ◽

Polygonum Cuspidatum

Dry eyes are caused by highly increased osmolarity of tear film, inflammation, and apoptosis of the ocular surface. In this study, we investigated the effect of Polygonum cuspidatum (PCE) aqueous extract in in vivo and in vitro dry eye models. Dry eye was induced by excision of the lacrimal gland and hyperosmotic media. In vivo, oral administration of PCE in exorbital lacrimal gland-excised rats recovered tear volume and Mucin4 (MUC4) expression by inhibiting corneal irregularity and expression of inflammatory cytokines. In vitro, hyperosmotic media induced human corneal epithelial cell (HCEC) cytotoxicity though increased inflammation, apoptosis, and oxidative stress. PCE treatment significantly inhibited expression of cyclooxygenase-2 and inflammatory cytokines (interleukin-6 and tumor necrosis factor-α), and activation of NF-κB p65 in hyperosmolar stress-induced HCECs. Hyperosmolarity-induced increase in Bcl-2-associated X protein (BAX) expression and activation of cleaved poly (ADP-ribose) polymerase and caspase 3 were attenuated in a concentration-dependent manner by PCE. PCE treatment restored anti-oxidative proteins such as heme oxygenase-1 (HO-1), superoxide dismutase-1 (SOD-1), and glutathione peroxidase (GPx) in hyperosmolar stress-induced HCECs. These data demonstrate that PCE prevents adverse changes in the ocular surface and tear fluid through inhibition of hyperosmolar stress-induced inflammation, apoptosis, and oxidation, suggesting that PCE may have the potential to preserve eye health.

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