scholarly journals A Rabbit Model of Aqueous-Deficient Dry Eye Disease Induced by Concanavalin A Injection into the Lacrimal Glands: Application to Drug Efficacy Studies

Author(s):  
Robert A. Honkanen ◽  
Liqun Huang ◽  
Basil Rigas
2018 ◽  
Vol 198 ◽  
pp. 58-72 ◽  
Author(s):  
Robert A. Honkanen ◽  
Liqun Huang ◽  
Gang Xie ◽  
Basil Rigas

2021 ◽  
Vol Volume 16 ◽  
pp. 3613-3631
Author(s):  
Liandi Huang ◽  
Huanhuan Gao ◽  
Zhigang Wang ◽  
Yixin Zhong ◽  
Lan Hao ◽  
...  

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0254036
Author(s):  
Adam Master ◽  
Apostolos Kontzias ◽  
Liqun Huang ◽  
Wei Huang ◽  
Anna Tsioulias ◽  
...  

The pathophysiology of dry eye disease (DED) remains largely unknown, accounting in part for the lack of successful treatments. We explored the pathophysiology of DED using a rabbit model of chronic DED induced with 3 weekly injections of Concanavalin A into the periorbital lacrimal glands. The transcriptome of full-thickness’s conjunctival tissue from rabbits with DED and from normal controls was determined using microarrays and, as needed, confirmatory real-time polymerase chain reactions. Results were subjected to bioinformatic analysis. DED induced large-scale changes in gene transcription involving 5,184 genes (22% of the total). Differentially expressed genes could be segregated into: functional modules and clusters; altered pathways; functionally linked genes; and groups of individual genes of known or suspected pathophysiological relevance to DED. A common feature of these subgroups is the breadth and magnitude of the changes that encompass ocular immunology and essentially all aspects of cell biology. Prominent changes concerned innate and adaptive immune responses; ocular surface inflammation; at least 25 significantly altered signaling pathways; a large number of chemokines; cell cycle; and apoptosis. Comparison of our findings to the limited extant transcriptomic data from DED patients associated with either Sjogren’s syndrome or non-Sjogren’s etiologies revealed a significant correlation between human and rabbit DED transcriptomes. Our data, establishing the large-scale transcriptomic changes of DED and their potential similarity to the human, underscore the enormous complexity of DED; establish a robust animal model of DED; will help expand our understanding of its pathophysiology; and could guide the development of successful therapeutic strategies.


Author(s):  
Isha Chandrakar ◽  
Shruti Sanghavi

Dry eye disease (DED) is a multifactorial disease in which the tear film’s homeostasis is lost, along with other ocular symptoms such as tear film instability and high osmolarity, neurosensory abnormalities, and ocular surface inflammation and damage. DED is a condition of lacrimal apparatus which is responsible for tear production. The tear film is a mixture of mucin, aqueous (water and solutes like NacI, sugar, urea, proteins,), lipids secreted by goblet cells, lacrimal glands, and meibomian glands, respectively. It keeps the eye moist, provides oxygen to the cornea, and has antibacterial properties. The lipid layer prevents the evaporation of the aqueous. DED is categorized into (i)Aqueous-tear deficiency, characterized by a deficiency of lacrimal glands to secrete tears, (ii)Evaporative DED, associated with increased tear loss by evaporation because there is a deficiency of the meibomian glands. The mechanism of DED might be loss of tear through evaporation or insufficient aqueous production or a combination of the two. DED is a widespread eye problem, which is often left untreated. It causes irritation, itching, dryness, foreign body sensation, and discomfort; severe case causes conjunctival congestion, keratinization, erosion of the corneal epithelium, and plaque formation. If left Univision- threatening vision-threatening, leading to complications like corneal ulceration and perforation. Various clinical tests are used to diose DED, including tear breakup time, tear osmolarity, Schirmer test, Rose Bengal staining, and expression of inflammatory markers. There is no cure for DED at present. The following modalities are used for its treatment: use of punctual and canalicular plugs, artificial tear products like polyethylene glycol/propylene glycol with guar HP, consuming food rich in omega-three fatty acids, antioxidants zeaxanthin, and lutein, Use of anti-inflammatory drugs, mucolytics, secretagogues. Reducing or avoiding mild risk factors like prolonged reading, prolonged use of contact lenses, excessive screen time, etc. Treatment of causative disease.  Appropriate management and establishing reasonable patient expectations are necessary to ensure patient satisfaction and adherence to the treatment.


2021 ◽  
Vol 62 (4) ◽  
pp. 14
Author(s):  
Yong Woo Ji ◽  
Hyun Goo Kang ◽  
Jong Suk Song ◽  
Ji Won Jun ◽  
Kyusun Han ◽  
...  

2021 ◽  
Vol 22 (21) ◽  
pp. 11820
Author(s):  
Yoko Ogawa ◽  
Tsutomu Takeuchi ◽  
Kazuo Tsubota

Autoimmune epithelitis and chronic inflammation are one of the characteristic features of the immune pathogenesis of Sjögren’s syndrome (SS)-related dry eye disease. Autoimmune epithelitis can cause the dysfunction of the excretion of tear fluid and mucin from the lacrimal glands and conjunctival epithelia and meibum from the meibomian glands. The lacrimal gland and conjunctival epithelia express major histocompatibility complex class II or human leukocyte antigen-DR and costimulatory molecules, acting as nonprofessional antigen-presenting cells for T cell and B cell activation in SS. Ocular surface epithelium dysfunction can lead to dry eye disease in SS. Considering the mechanisms underlying SS-related dry eye disease, this review highlights autoimmune epithelitis of the ocular surface, chronic inflammation, and several other molecules in the tear film, cornea, conjunctiva, lacrimal glands, and meibomian glands that represent potential targets in the treatment of SS-related dry eye disease.


2019 ◽  
Vol 44 (8) ◽  
pp. 863-872 ◽  
Author(s):  
Robert Honkanen ◽  
Wei Huang ◽  
Liqun Huang ◽  
Kevin Kaplowitz ◽  
Sarah Weissbart ◽  
...  

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