scholarly journals Sjögren’s Syndrome-Like Ocular Surface Disease in Thrombospondin-1 Deficient Mice

2009 ◽  
Vol 175 (3) ◽  
pp. 1136-1147 ◽  
Author(s):  
Bruce Turpie ◽  
Takeru Yoshimura ◽  
Abha Gulati ◽  
Jose David Rios ◽  
Darlene A. Dartt ◽  
...  
Keyword(s):  
Sjögren’S Syndrome ◽  
Ocular Surface ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Ocular Surface Disease ◽  
Thrombospondin 1 ◽  
Deficient Mice ◽  
Sjögren‘S Syndrome

scholarly journals Thrombospondin-1 Is Necessary for the Development and Repair of Corneal Nerves

2018 ◽  
Vol 19 (10) ◽  
pp. 3191 ◽  
Author(s):  
Yukako Tatematsu ◽  
Qalbi Khan ◽  
Tomas Blanco ◽  
Jeffrey Bair ◽  
Robin Hodges ◽  
...  
Keyword(s):  
Confocal Microscopy ◽  
Sjögren’S Syndrome ◽  
Dry Eye ◽  
Ocular Surface ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Corneal Nerves ◽  
Thrombospondin 1 ◽  
Sjögren‘S Syndrome

Thrombospondin-1-deficient (TSP-1−/−) mice are used as an animal model of Sjögren’s Syndrome because they exhibit many of the symptoms associated with the autoimmune type of dry eye found in primary Sjögren’s Syndrome. This type of dry eye is linked to the inflammation of the lacrimal gland, conjunctiva, and cornea, and is thought to involve dysfunction of the complex neuronal reflex arc that mediates tear production in response to noxious stimuli on the ocular surface. This study characterizes the structural and functional changes to the corneal nerves that are the afferent arm of this arc in young and older TSP-1−/− and wild type (WT) mice. The structure and subtype of nerves were characterized by immunohistochemistry, in vivo confocal microscopy, and confocal microscopy. Cytokine expression analysis was determined by Q-PCR and the number of monocytes was measured by immunohistochemistry. We found that only the pro-inflammatory cytokine MIP-2 increased in young corneas of TSP-1−/− compared to WT mice, but tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-2 (MIP-2) all increased in older TSP-1−/− mouse corneas. In contrast, CD11b+ pro-inflammatory monocytes did not increase even in older mouse corneas. Calcitonin gene-related peptide (CGRP)-, but not Substance P (SubP)-containing corneal nerves decreased in older, but not younger TSP-1−/− compared to WT mouse corneas. We conclude that CGRP-containing corneal sensory nerves exhibit distinct structural deficiencies as disease progresses in TSP-1−/− mice, suggesting that: (1) TSP-1 is needed for the development or repair of these nerves and (2) impaired afferent corneal nerve structure and hence function may contribute to ocular surface dysfunction that develops as TSP-1−/− mice age.

Differential Diagnosis of Dry Eye Conditions

1996 ◽  
Vol 10 (1) ◽  
pp. 9-12 ◽  
Author(s):  
S.C. Pflugfelder
Keyword(s):  
Sjögren’S Syndrome ◽  
Dry Eye ◽  
Ocular Surface ◽  
Sjögren's Syndrome ◽  
Keratoconjunctivitis Sicca ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Ocular Surface Disease ◽  
Mucin Production ◽  
Sjögren‘S Syndrome

The pre-ocular tear film is a complex biochemical structure produced by the lacrimal glands and epithelial cells on the ocular surface. Clinical syndromes of ocular irritation may result from deficiencies in one or more of these layers. At a recent dry eye workshop at the National Eye Institute, dry eye conditions were classified into those with adequate aqueous tear production and those with aqueous tear deficiency. The majority of patients with aqueous adequate dry eye suffer from meibomian gland dysfunction that results in lipid tear deficiency. Aqueous tear deficiency can be subclassified into non-Sjogren's syndrome and Sjogren's syndrome (SS) groups. Patients with non-Sjögren's aqueous tear deficiency have less-severe symptoms and ocular surface disease than those with SS. The etiology of non-Sjögren's aqueous tear deficiency has not been established, but it appears to be multifactorial. In SS, immune-mediated destruction of the lacrimal gland results in severe aqueous tear deficiency. Aqueous tear deficiencies lead to ocular surface disease, termed keratoconjunctivitis sicca (KCS). KCS results from abnormal terminal differentiation of the ocular surface epithelia and is associated with marked reduction in mucin production by these cells. Clinical features helpful in differentiating the various dry eye syndromes are reviewed.

scholarly journals TLR7 Signaling Drives the Development of Sjögren’s Syndrome

2021 ◽  
Vol 12 ◽  
Author(s):  
Yawen Wang ◽  
Annie Roussel-Queval ◽  
Lionel Chasson ◽  
Noël Hanna Kazazian ◽  
Laetitia Marcadet ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Autoimmune Disease ◽  
Salivary Glands ◽  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Autoantibody Production ◽  
Deficient Mice ◽  
Sjögren‘S Syndrome

Sjögren’s syndrome (SS) is a chronic systemic autoimmune disease that affects predominately salivary and lacrimal glands. SS can occur alone or in combination with another autoimmune disease like systemic lupus erythematosus (SLE). Here we report that TLR7 signaling drives the development of SS since TLR8-deficient (TLR8ko) mice that develop lupus due to increased TLR7 signaling by dendritic cells, also develop an age-dependent secondary pathology similar to associated SS. The SS phenotype in TLR8ko mice is manifested by sialadenitis, increased anti-SSA and anti-SSB autoantibody production, immune complex deposition and increased cytokine production in salivary glands, as well as lung inflammation. Moreover, ectopic lymphoid structures characterized by B/T aggregates, formation of high endothelial venules and the presence of dendritic cells are formed in the salivary glands of TLR8ko mice. Interestingly, all these phenotypes are abrogated in double TLR7/8-deficient mice, suggesting that the SS phenotype in TLR8-deficient mice is TLR7-dependent. In addition, evaluation of TLR7 and inflammatory markers in the salivary glands of primary SS patients revealed significantly increased TLR7 expression levels compared to healthy individuals, that were positively correlated to TNF, LT-α, CXCL13 and CXCR5 expression. These findings establish an important role of TLR7 signaling for local and systemic SS disease manifestations, and inhibition of such will likely have therapeutic value.

Measuring the Lacunar Sulci as a New Indicator of Shrinkage of the Ocular Surface

2001 ◽  
Vol 11 (3) ◽  
pp. 227-232 ◽  
Author(s):  
J. Murube ◽  
L. Chenzhuo ◽  
E. Murube ◽  
L. Rivas ◽  
O. Shalaby
Keyword(s):  
Sjögren’S Syndrome ◽  
Ocular Surface ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Vanishing Point ◽  
Cicatricial Pemphigoid ◽  
Ocular Cicatricial Pemphigoid ◽  
Healthy Persons ◽  
Sjögren‘S Syndrome

Purpose To present a new indicator that measures the sulci of the lacrimal lake of the eye according to the degrees of ocular abduction at which they vanish. This new approach will help determine the severity and progression of mucosal retraction in ocular surface diseases. Methods A total of 181 eyes of 94 healthy persons, 130 eyes of 65 patients with Sjögren's syndrome, and 30 eyes of 15 patients with ocular pemphigoid were examined using the slit lamp. We recorded the vanishing point of the three main lacunar sulci (plico-bulbar, plico-caruncular and dermo-caruncular) while abducting. Results In healthy persons, the average vanishing points for the first and second lacunar sulci were respectively, 53.2° ± 12.3 and 54.5° ± 9.8. In patients with Sjögren's syndrome, 49.53° ± 10.81 and 53.17° ± 7.28 and in patients with incipient ocular cicatricial pemphigoid, 42.69° ± 14.33 and 44.46° ± 16.85. Statistical significance was p < 0.005. Conclusions The lacunar sulci are shallower and vanish sooner in ocular cicatricial pemphigoid and Sjögren syndrome than in normals. Investigating the vanishing point of the lacunar sulci while abducting is useful for grading the shrinkage of the conjunctiva, caruncle and medial canthus.

scholarly journals Development of Autoimmune Exocrinopathy Resembling Sjögren's Syndrome in Estrogen-Deficient Mice of Healthy Background

2003 ◽  
Vol 163 (4) ◽  
pp. 1481-1490 ◽  
Author(s):  
Naozumi Ishimaru ◽  
Rieko Arakaki ◽  
Megumi Watanabe ◽  
Masaru Kobayashi ◽  
Katsushi Miyazaki ◽  
...  
Keyword(s):  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Autoimmune Exocrinopathy ◽  
Deficient Mice ◽  
Sjögren‘S Syndrome

scholarly journals Modulation of Conjunctival Goblet Cell Function by Inflammatory Cytokines

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
L. Contreras-Ruiz ◽  
A. Ghosh-Mitra ◽  
M. A. Shatos ◽  
D. A. Dartt ◽  
S. Masli
Keyword(s):  
Sjögren’S Syndrome ◽  
Inflammatory Cytokines ◽  
Goblet Cell ◽  
Ocular Surface ◽  
Cell Function ◽  
Sjögren's Syndrome ◽  
Goblet Cells ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Sjögren‘S Syndrome

Ocular surface inflammation associated with Sjögren’s syndrome is characterized by a loss of secretory function and alteration in numbers of mucin secreting goblet cells. Such changes are a prominent feature of ocular surface inflammatory diseases and are attributed to inflammation; however, the exact effect of the inflammatory cytokines on conjunctival goblet cell function remains largely unknown. In this study, we developed a primary culture of mouse goblet cells from conjunctival tissue and evaluated the effects on their function by inflammatory cytokines detected in the conjunctiva of mouse model of Sjögren’s syndrome (Thrombospondin-1 deficient mice). We found that apoptosis of goblet cells was primarily induced by TNF-αand IFN-γ. These two cytokines also inhibited mucin secretion by goblet cells in response to cholinergic stimulation, whereas IL-6 enhanced such secretion. No changes in secretory response were detected in the presence of IL-13 or IL-17. Goblet cells proliferated to varying degrees in response to all the tested cytokines with the greatest response to IL-13 followed by IL-6. Our results therefore reveal that inflammatory cytokines expressed in the conjunctiva during an ocular surface disease directly disrupt conjunctival goblet cell functions, compromising the protective function of tears, thereby contributing to ocular surface damage.

scholarly journals Ocular Surface Disease in Sjögren's Syndrome: Management in a Scleral Lens Clinical Practice

2020 ◽  
Vol 4 (1) ◽  
pp. e12-e22
Author(s):  
Daddi Fadel ◽  
Melissa Barnett
Keyword(s):  
Quality Of Life ◽  
Sjögren’S Syndrome ◽  
Dry Eye ◽  
Ocular Surface ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Autologous Serum ◽  
Sjögren‘S Syndrome

Sjögren’s syndrome is a chronic, autoimmune, systemic disease characterized by lymphocytic infiltration and malfunction of the exocrine glands, primarily the lacrimal and salivary glands, resulting in predominant symptoms of dry eye and dry mouth. Sjögren’s syndrome is a highly prevalent condition and is one of the most common systemic, rheumatic, autoimmune diseases, affecting up to 1.4% of adults in the United States, second only to rheumatoid arthritis in its prevalence in North America. Primary Sjögren’s syndrome has shown to affect patients’ health-related quality-of-life due to dryness, chronic pain, depression, anxiety,physical and mental fatigue, and neuropsychiatric symptoms. Scleral lenses (SLs) have shown to be significantly beneficial in relieving symptoms and improvingquality-of-life in patients with Sjögren’s syndrome and dry eye disease. SLs may be used concurrently with the other therapies including ocular lubricants, eyelid hygiene, punctal occlusion, topical prescription medications, and autologous serum. This manuscript reviews the implication of Sjögren’s syndrome on the ocular surface and quality-of-life and describes how SLs, in combination with other treatments, may be beneficial.

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