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At least 361 records · Page 20Linked to original sources

PubMed1997

Limbal conjunctival Langerhans cell density in ocular cicatricial pemphigoid: an indirect immunofluorescence study on Dispase-split conjunctiva.

PURPOSE: To evaluate limbal conjunctival Langerhans cell density in ocular cicatricial pemphigoid patients versus normal controls. Langerhans cells obviously play a major role in T-cell activation and are involved in corneal and conjunctival inflammatory diseases. METHODS: We used a protease (Dispase II) on inferior limbal conjunctival biopsies to separate the epithelium from the substantia propria and performed indirect immunofluorescence to analyze CD1a+ (a specific Langerhans cell surface antigen) cell density on flat-mounted epithelial sheets obtained from 30 normal controls and 11 patients presenting with ocular cicatricial pemphigoid. RESULTS: This technique was quick and reproducible. The mean Langerhans cell density in normal limbal conjunctiva was 272 +/- 37 cells/mm2. It was significantly higher in ocular cicatricial pemphigoid patients: 386 +/- 43 cells/mm2 (p = 0.001). CONCLUSIONS: Conjunctival Langerhans cell density in ocular surface inflammatory diseases can best be evaluated by indirect immunofluorescence, following epithelial sheet separation from the substantia propria, using Dispase II.

Aged↗

PubMed2004

Inflammation in dry eye.

Dry eye is a condition of altered tear composition that results from a diseased or dysfunctional lacrimal functional unit. Evidence suggests that inflammation causes structural alterations and/or functional paralysis of the tear-secreting glands. Changes in tear composition resulting from lacrimal dysfunction, increased evaporation and/or poor clearance have pro-inflammatory effects on the ocular surface. This inflammation is responsible in part for the irritation symptoms, ocular surface epithelial disease, and altered corneal epithelial barrier function in dry eye. Anti-inflammatory therapies for dry eye target one or more of the inflammatory mediators/pathways that have been identified in dry eye.

Journal Article↗

PubMed2004

Antiinflammatory therapy for dry eye.

PURPOSE: To present evidence establishing the relationship between inflammation and dry eye and supporting the use of antiinflammatory therapy for dry eye. DESIGN: Analysis of literature. METHODS: Research studies that evaluated inflammation in dry eye pathogenesis and clinical trials of antiinflammatory therapies for dry eye were reviewed. RESULTS: There is increasing evidence that decreased tear secretion, decreased tear turnover, and desiccation promote inflammation on the ocular surface. An increase in soluble mediators (cytokines and proteases) in the tear fluid, adhesion molecule expression by the conjunctival epithelium, and T-cell infiltration of the conjunctiva have been observed in dry eye patients. This inflammation appears to have a role in the pathogenesis of the ocular surface epithelial disease, termed keratoconjunctivitis sicca (KCS), that develops in dry eye. Clinical improvement of KCS has been observed after therapy with antiinflammatory agents including corticosteroids, cyclosporin and doxycycline. Cyclosporin A emulsion was approved by the Food and Drug Administration as therapy for dry eye. Randomized placebo-controlled FDA clinical trials showed that cyclosporine A was superior to vehicle in stimulating aqueous tear production, decreasing corneal punctuate fluorescein staining, reducing symptoms of blurred vision, and decreasing artificial tear use in patients with KCS. No ocular or systemic toxicity was observed from this medication. CONCLUSIONS: Ocular surface and lacrimal gland inflammation has been identified in dry eye that plays a role in the pathogenesis of KCS. Antiinflammatory therapy has efficacy for treating KCS. Cyclosporin A is the first FDA approved therapy for this indication. It improved signs and symptoms of KCS, and it is safe for long-term use.

Anti-Inflammatory Agents↗

PubMedDate not supplied

Corneal keratinization in the oel/ + mouse.

Several human diseases are accompanied by keratinization of the ocular surface and loss of corneal transparency. We describe a mouse strain in which 2/3 of the viable offspring manifest a corneal disease characterized initially by poor wetting followed by keratinization of the ocular surface, and progressive loss of corneal transparency. The corneal epithelium becomes vacuolated and the basement membrane thickened. Ulceration and perforation were seen in some cases. Standard bacterial cultures yielded no culpable pathogens. Blood antiviral titers and cultures of orbital and ocular tissues for herpes virus were negative. Double masked treatment trials with topical gentamicin, and topical and parenteral vitamin A had no significant effect on the course of the disease. The mouse strain exhibits corneal keratinization unresponsive to vitamin A therapy, and may serve as an excellent model of certain serious human ocular surface diseases.

Animals↗

PubMed1998

Tear dynamics and dry eye.

Tears undergo four processes: production by the lacrimal gland, distribution by blinking, evaporation from the ocular surface and drainage through the nasolacrimal duct. Abnormalities in any of these steps can cause dry eye. There are two kinds of tear production, basic and reflex, which can be distinguished from each other by the Schirmer test with nasal stimulation. Reflex tearing is important because it supplies such essential components as EGF and vitamin A, whose deficiency may cause squamous metaplasia. There is no reflex tearing in Sjogren's syndrome because of destruction of the lacrimal gland. In cases of diminished or absent reflex tearing, topical autologous serum is the treatment of choice. Even when there is adequate tear production, insufficient distribution, such as occurs with the decreased blinking associated with the use of video display terminals (VDT), may cause dry eye. Any process or activity that suppresses blinking interferes with tear distribution. Tear evaporation increases under certain conditions and in some diseases. When the exposed ocular surface area is increased, such as in VDT work, tear evaporation increases. Meibomian gland dysfunction (MGD) also causes increased tear evaporation by altering the quality of the oily layer in tears. Tear evaporation can be suppressed by using a warm compresser or a humidifier, narrowing the palpebral fissure, or wearing protective eyeglasses. The tear clearance rate is measured by fluorescein dye dilution in the conjunctiva. When the tear clearance is low, inflammatory cytokines or preservatives accumulate in the conjunctival sac, resulting in ocular surface diseases. Frequent use of artificial tears without preservative is the key treatment. A differential diagnosis of the abnormalities of tear dynamics can give us a proper understanding of the pathogenesis of dry eye. With this knowledge, we can formulate an efficient therapeutic approach.

Blinking↗

PubMedDate not supplied

[Ocular surface analysis in patients affected with rheumatic diseases].

OBJECTIVE: The international criteria for primary Sjögren's Syndrome (SS I) diagnosis (Vitali et al. 2002) include the Schirmer test I and vital dye staining as tests for ocular surface involvement, but diagnosis can be reached also when the item for ocular signs is not satisfied. The purpose of our study was to evaluate the ocular surface in patients with Sjögren's Syndrome, non-Sjögren's autoimmune diseases and Sicca Syndrome, to understand whether the SS I diagnosis can be targeted also on other tests related to the ocular surface status. METHODS: Clinical and cytological data were collected from 122 patients: 40 patients had diagnosis of Primary Sjögren's Syndrome, 51 a non Sjögren's autoimmune disease and 31 had symptoms of dry eye. A validated questionnaire on symptoms was filled by each patient; clinical tests included: Schirmer test I, Jones test, Ferning test, Break Up Time, corneal aesthesiometry, tear clearance test, vital dye staining of the ocular surface, scraping and impression conjunctival cytology. Data were statistically evaluated by using SPSS software and Mann-Whitney analysis on unpaired data. RESULTS: Data show that the subjective symptoms score, tear production, tear turnover, corneal sensitivity and ocular surface integrity are affected in SS I patients, with a statistically significant difference when matched to the other two groups. CONCLUSIONS: Our results suggest to enlarge the spectrum of ocular surface analysis, to support and orient a differential diagnosis among the autoimmune diseases.

Arthritis, Rheumatoid↗

PubMed2004

Distribution of mucins at the ocular surface.

Mucins are vital for maintenance of a healthy, wet ocular surface. Once only thought to be secreted by goblet cells, mucins are now also known to be of the membrane-associated type. Stratified ocular surface epithelia express at their apical-tear fluid surface a repertoire of membrane-associated mucins including MUC1, MUC4, MUC16. These mucins are concentrated on the tips of the microplicae, forming a dense glycocalyx at the epithelial tear film interface. A major mucin of the secretory class is the goblet-cell-derived gel-forming mucin MUC5AC. A small soluble mucin, MUC7, is expressed by the lacrimal gland acini. Our hypothesis of the role/distribution of the secreted and membrane-associated mucins at the ocular surface is that the secreted mucins are soluble in the tear fluid, and are moved about and shunted to the nasolacrimal duct and by the eyelids during blinking. Thus, in the tears, the secreted mucins act as clean-up/debris removing multimeric networks that at the same time, through their hydrophilic nature, hold fluids in place and harbor defense molecules secreted by the lacrimal gland. Membrane-associated mucins, on the other hand, form a dense barrier in the glycocalyx at the epithelial tear film interface. This barrier prevents pathogen penetrance and is a lubricating surface that allows lid epithelia to glide over the corneal epithelia without adherence. The secreted mucins move easily over the glycocalyx mucins because both have anionic character that creates repulsive forces between them. Little is known regarding regulation of expression and glycosylation of mucins by ocular surface epithelia. Since ocular surface drying diseases alter both goblet cell and mucin production, and production and glycosylation of membrane-associated mucins, studies of mucin gene regulation and glycosylation may yield treatment modalities for these diseases.

Conjunctiva↗

PubMed1995

Measurement of IL-4 in tears of patients with seasonal allergic conjunctivitis and vernal keratoconjunctivitis.

To elucidate the mechanism of ocular surface allergic disease, we focused on IL-4, which is one of the key factors in regulating IgE production, and thus determined the concentration of IL-4 in tears. IL-4 concentration was determined in the tears of 15 patients with seasonal allergic conjunctivitis, 15 vernal keratoconjunctivitis (VKC), 10 giant papillary conjunctivitis (GPC), 10 patients with non-allergic conjunctivitis and post-cataract surgical conjunctivitis as intermediate conjunctivitis, and 10 normal subjects using a highly sensitive sandwich ELISA. The mean level of IL-4 in normal controls was low, and seasonal allergic conjunctivitis, VKC and GPC showed a significant elevation (P < 0.05), respectively. IL-4 of VKC and GPC were also significantly higher than allergic conjunctivitis, and non-allergic conjunctivitis and post-cataract surgical conjunctivitis were not higher than normal. These results raise the possibility that the increased level of IL-4 in tears could play a role in allergic disease and its severity in patients.

Adolescent↗

PubMed1999

Culture and characterisation of epithelial cells from human pterygia.

BACKGROUND/AIMS: Pterygia are a common disorder of the ocular surface. The disease represents a chronic fibrovascular and degenerative process thought to originate at the conjunctival-corneal junction, where altered limbal stem cells are proposed to be the cell of origin. Extensive epidemiological evidence exists to implicate ultraviolet B irradiation in the pathogenesis of pterygia. To date no animal or in vitro culture model has been developed to test such an hypothesis. The aim of this study was to establish and characterise a pure population of epithelial cells derived from pterygium tissue. METHODS: Tissue specimens were obtained from patients undergoing pterygium excision. Explants were cultured in either serum free or serum supplemented medium. Primary and passaged cells were processed for light microscopy, analysed by flow cytometry, and characterised immunohistochemically using specific antibodies. RESULTS: In serum free culture, cuboidal cells with typical morphology of epithelial cells migrated from the pterygium explants from 3 days onwards and eventually formed a cohesive monolayer. Passaged cells consisted of 98.4% cytokeratin positive cells and demonstrated immunoreactivity for multiple cytokeratins, including AE1, AE3, AE5, but were negative for AE8. These cells also expressed an epithelial specific antigen, together with vimentin and mucin, as did epithelial cells in sections of pterygia. CONCLUSIONS: A relatively simple method of isolating pterygium epithelial cells has been established. Cultured pterygium epithelial cells are phenotypically and functionally similar to their in vivo counterparts with respect to keratin, vimentin, and mucin expression. In vitro assays using these cells may aid in elucidating the pathogenesis of pterygia.

Cells, Cultured↗

PubMed2000

Doxycycline inhibition of interleukin-1 in the corneal epithelium.

PURPOSE: To evaluate the effect of doxycycline on the regulation of interleukin (IL)-1 expression and activity in human cultured corneal epithelium. METHODS: Human corneal limbal epithelium (HLE) was cultured from explants prepared from limbal rings of donor corneas. Primary cultured limbal epithelial cells were treated with either 10 microg/ml lipopolysaccharide (LPS), LPS with 10 microg/ml doxycycline, or LPS with 0.1 mg/ml methylprednisolone (MP) for 24 hours. The intracellular and supernatant protein amounts of IL-1alpha, the precursor and mature forms of IL-1beta, IL-1 receptor antagonist (IL-1 RA), and the intracellular level of IL-1beta-converting enzyme (ICE) were measured with enzyme-linked immunosorbent assays (ELISAs). Western blot analysis was performed to evaluate IL-1 RA protein. mRNA steady state amounts were determined by RNase protection assay (RPA) for IL-1alpha, IL-1beta, IL-1 RA, and ICE. RESULTS: LPS increased the mRNA and protein amounts of intracellular and released IL-1alpha, mature IL-1beta, and IL-1 RA. Doxycycline inhibited the LPS-induced IL-1beta increase in the mRNA and protein amounts in the corneal epithelium and upregulated the expression of the anti-inflammatory IL-1 RA protein. In addition, doxycycline reduced the steady state level of the cellular ICE protein but did not affect the level of ICE transcripts. IL-1beta secreted to the conditioned media of HLE was functionally active in inducing matrix metalloproteinase (MMP)-1 and MMP-3 in cultured corneal fibroblasts. Doxycycline significantly decreased IL-1beta bioactivity in the supernatants from LPS-treated corneal epithelial cultures. These effects were comparable to those induced by the corticosteroid, MP. CONCLUSIONS: Doxycycline can suppress the steady state amounts of mRNA and protein of IL-beta and decrease the bioactivity of this major inflammatory cytokine. These data may partially explain the clinically observed anti-inflammatory properties of doxycycline. The observation that doxycycline was equally potent as a corticosteroid, combined with the relative absence of adverse effects, makes it a potent drug for a wide spectrum of ocular surface inflammatory diseases.

Anti-Bacterial Agents↗

PubMed2002

[N acetyl-aspartyl glutamic acid (NAAGA) inhibits the adhesion of leukocytes to activated endothelial cells and down-modulates the cytokine-induced expression of adhesion molecules].

BACKGROUND: Cell adhesion plays a pivotal role in most ocular surface inflammatory diseases. Adhesion molecules mediate cell-to-cell and cell-to-matrix adhesion. Their expression is up-regulated by pro-inflammatory stimuli such as cytokines, histamine or complement-derived anaphylatoxins. The dipeptide N acetyl-aspartyl glutamic acid (NAAGA) is used as unpreserved topical eyedrops in the treatment of allergic conjunctivitis. NAAGA is known to inhibit leukotriene synthesis, histamine release by mast cells, and complement-derived anaphylatoxin production. PURPOSE: To investigate the potential capability of NAAGA to interfere with leukocyte adhesion to endothelial cells and modulate cytokine-induced expression of adhesion molecules. METHODS: Human blood-derived leukocytes were co-cultured with human umbilical vein endothelial cells (HUVECs) in the absence or the presence of 1000 UI/mL human recombinant TNFalpha, 10(-4) M histamine di-hydrochloride or 5x10(-6) M human recombinant C5a, and in the absence or presence of NAAGA (final concentration 2.45%). Adhesion of leukocytes to HUVECs was calculated by subtracting the number of nonadherent leukocytes from the total number of leukocytes. Expression of adhesion molecules was assessed by flow cytometry using anti-CD11b, anti-CD49d, anti-ICAM-1 (CD54), anti-ICAM-2 (CD102), anti-VCAM-1 (CD106) and anti-ELAM-1 (CD62E) monoclonal antibodies. RESULTS: NAAGA was found to totally inhibit adhesion of unstimulated leukocytes, or leukocytes activated with C5a, TNFalpha, or histamine, to TNFalpha-stimulated HUVECs (P=0.0001). Adhesion of leukocytes to unstimulated HUVECs was not modified by NAAGA. Similar results were obtained with endothelial cells stimulated by histamine or C5a. Taken together, these data indicate that NAAGA totally abrogates cell adhesion under inflammatory conditions, without interfering with the physiological adhesion of leukocytes to normal endothelium. At the molecular level, NAAGA inhibited histamine-induced expression of CD11b (P=0.0004) and CD49d (P=0.0045) on granulocytes. On TNFalpha-activated HUVECs, NAAGA induced a significant decrease in the VCAM-1 expression level (P<0.0001) and totally reversed TNFalpha-induced overexpression of ICAM-1 (P=0.0069), ICAM-2 and ELAM-1 (P<0.0001), without interfering with baseline expression of these molecules. CONCLUSION: These results show that the antiallergic compound NAAGA directly inhibits leukocyte adhesion to endothelial cells induced by pro-inflammatory stimuli, and abrogates TNFalpha-induced expression of adhesion molecules on granulocytes and endothelial cells. This capacity to block overexpression of selectins and integrins induced by pro-inflammatory stimuli confers to NAAGA a potential as an anti-inflammatory drug, since interfering with adhesion molecule expression is probably one of the most efficient ways to curb leukocyte recruitment to inflammatory sites.

Antigens, CD↗

PubMed2005

[Effect of doxycycline on inflammation-related cytokines and apoptosis in human conjunctival epithelial cells].

OBJECTIVE: To evaluate the effects of doxycycline on the regulation of intercellular adhesion molecule-1 (ICAM-1, CD54), interleukin-1beta (IL-1beta), human leukocyte antigen DR (HLA-DR) and apoptosis in human conjunctival epithelial cells. METHODS: Human primary conjunctival epithelial cells were isolated and cultured from donors and identified by immunohistochemistry. Cultured epithelial cells were treated with either 0 U/ml IFN-gamma, 300 U/ml IFN-gamma, 300 U/ml IFN-gamma with 10 microg/ml doxycycline, 300 U/ml IFN-gamma with 20 microg/ml doxycycline, 300 U/ml IFN-gamma with 40 microg/ml doxycycline or 300 U/ml IFN-gamma with 100 microg/ml dexamethasone for 24 hours. The amount of CD54, HLA-DR and IL-1beta was measured by flow cytometry and western blot analysis. Apoptosis was evaluated by flow cytometry after the cultured epithelial cells were treated for 72 hours. RESULTS: Cultured conjunctival epithelial cells can express CD54 and IL-1beta. IFN-gamma increased the amount of CD54 and IL-1beta (P < 0.01). Doxycycline and dexamethasone inhibited the IFN-gamma induced increase of express of CD54 and IL-1beta of cultured conjunctival epithelial cells, and the inhibiting effect was dependent on the concentration of doxycycline (P < 0.01). Very little HLA-DR and apoptosis were detected before and after treatment with IFN-gamma. CONCLUSION: Doxycycline can suppress the expression of inflammatory cytokine such as CD54 and IL-1beta, which suggests that doxycycline may be a potent drug for the treatment of ocular surface inflammatory disease.

Anti-Bacterial Agents↗

PubMedDate not supplied

[Amnion and ocular surface problems].

The amniotic membrane, the most internal placental membrane, has various properties useful in ophthalmology. Collected on delivery by elective Caesarean section, the amnion is prepared under sterile conditions, and, usually, cryopreserved until its use as a biological bandage or as a substrate for epithelial growth in the management of various ocular surface conditions. Specifically, the amnion is used to : (1) limit formation of adhesive bands between eyelids and eyeball (symblepharon) or the progression of a fibrovascular outgrowth towards the cornea (pterygium) or to (2) facilitate the healing of corneal ulcers, bullous keratopathy, and corneal stem cell deficiency. In this last condition, either hereditary or acquired after a thermal or a chemical burn, corneal stem cells, located at a transitional zone between the cornea and conjunctiva, are lost. These cells are essential for renewal of corneal epithelium in normal and in diseased states. The loss of these cells leaves the corneal surface free for invasion by conjunctival epithelium. Not only, does conjunctival epithelium support the development of vascularisation on the normally avascular cornea, but some conjunctival cells differentiate into mucus secreting goblet cells. Such a change in phenotype leads to loss of corneal transparency and visual disability. The removal of this fibro-vascular outgrowth in combination with transplantation of both amniotic membrane and corneal stem cells are used to treat this condition. The amnion stimulates the proliferation of less differentiated cells which have the potential to reconstruct the cornea. This potential is at the origin of the hypothesis that the amnion may provide an alternative niche for limbal stem cells of the corneal epithelium. It abounds in cytokines and has antalgic, anti-bacterial, anti-inflammatory and anti-immunogenic properties, in addition to allowing, like fetal skin does, wound healing with minimal scar formation. These desirable properties are responsible for the increasing use of amniotic membrane in ophthalmology. The complete understanding of the mechanisms of action of amniotic membrane for ocular surface diseases has yet to be understood. Once revealed by research, they may provide new pharmacological avenues to treat ocular surface diseases.

Amnion↗

PubMed2006

Increased risk for herpetic eye disease in patients with allergic conjunctivitis.

PURPOSE: To evaluate the risk of ocular surface herpetic eye disease (osHED) in allergic eye disease. METHODS: We calculated the risk for osHED in 11,205 patients on antiallergic ocular topical agents compared with 453,069 controls based on filled prescriptions for topical acyclovir between 2001 and 2003. RESULTS: Significantly more allergic patients, of all age groups, received treatment for osHED (p < 0.01). The age and gender adjusted relative risk for allergic patients to suffer an osHED event was 2.31 (95% CI: 1.84-2.90), raising to 3.55 (95% CI: 2.0-6.4) in patients that filled > or = 4 antiallergic prescriptions. CONCLUSIONS: Patients treated for allergic eye disease have an increased risk of osHED.

Acyclovir↗

PubMed1983

Ocular surface drying and tear film osmolarity in thyroid eye disease.

Five factors potentially associated with corneal exposure--palpebral fissure width, exophthalmos, blink rate, lagophthalmos, and lid lag--were evaluated in 17 patients with Graves' disease to determine which were associated with ocular surface damage. Multiple regression analysis revealed that increased palpebral fissure width and increased blink rate were both significant predictors of ocular surface damage (as measured by rose Bengal staining). Tear osmolarity and tear film break-up time were measured to determine the type of drying mechanism involved in thyroid eye disease. All eyes examined except one had blink rates adequate to prevent dry-spot formation. Fourteen of 33 eyes had abnormally high tear osmolarity. Increasing palpebral fissure width and increasing blink rate were both significant predictors of elevated osmolarity in tears obtained from the inferior marginal tear strip. We suspect that increased palpebral fissure width accelerates tear film evaporation, thus increasing tear film osmolarity with resultant ocular surface damage.

Adult↗

PubMed1998

The pathology of dry eye: the interaction between the ocular surface and lacrimal glands.

BACKGROUND: Most dry-eye symptoms result from an abnormal, nonlubricative ocular surface that increases shear forces under the eyelids and diminishes the ability of the ocular surface to respond to environmental challenges. This ocular-surface dysfunction may result from immunocompromise due to systemic autoimmune disease or may occur locally from a decrease in systemic androgen support to the lacrimal gland as seen in aging, most frequently in the menopausal female. HYPOTHESIS: Components of the ocular surface (cornea, conjunctiva, accessory lacrimal glands, and meibomian glands), the main lacrimal gland, and interconnecting innervation act as a functional unit. When one portion is compromised, normal lacrimal support of the ocular surface is impaired. Resulting immune-based inflammation can lead to lacrimal gland and neural dysfunction. This progression yields the OS symptoms associated with dry eye. THERAPY: Restoration of lacrimal function involves resolution of lymphocytic activation and inflammation. This has been demonstrated in the MRL/lpr mouse using systemic androgens or cyclosporine and in the dry-eye dog using topical cyclosporine. The efficacy of cyclosporine may be due to its immunomodulatory and antiinflammatory (phosphatase inhibitory capability) functions on the ocular surface, resulting in a normalization of nerve traffic. CONCLUSION: Although the etiologies of dry eye are varied, common to all ocular-surface disease is an underlying cytokine/receptor-mediated inflammatory process. By treating this process, it may be possible to normalize the ocular surface/lacrimal neural reflex and facilitate ocular surface healing.

Animals↗

PubMed2005

Allergic conjunctivitis: update on pathophysiology and prospects for future treatment.

Allergic conjunctivitis is in actuality a group of diseases affecting the ocular surface and is usually associated with type 1 hypersensitivity reactions. Two acute disorders, seasonal allergic conjunctivitis and perennial allergic conjunctivitis, exist, as do 3 chronic diseases, vernal keratoconjunctivitis, atopic keratoconjunctivitis, and giant papillary conjunctivitis. The ocular surface inflammation (usually mast cell driven) results in itching, tearing, lid and conjunctival edema-redness, and photophobia during the acute phase and can lead to a classic late-phase response (with associated eosinophilia and neutrophilia) in a subset of individuals. As is the case in other allergic diseases, a chronic disease can also develop, accompanied by remodeling of the ocular surface tissues. In severe cases the patient experiences extreme discomfort and sustains damage to the ocular surface. For such cases, there is no highly effective and safe treatment regimen. Topical administration of corticosteroids is used in severe cases but is associated with an increased risk for the development of cataracts and glaucoma. Thus there is a worldwide search for new biotargets for the treatment of these diseases. Here we provide a brief update of the clinical symptoms associated with these diseases, the rationale for disease classification, recent advances in our understanding of the pathogenesis of the diseases, and an update on both preclinical and clinical advances toward refined therapies for these diseases.

Administration, Topical↗

PubMed1997

Improved impression cytology techniques for the immunopathological diagnosis of superficial viral infections.

BACKGROUND: For epidemiological and therapeutic reasons early diagnosis of superficial viral infections is crucial. Conventional microbiological techniques are expensive, time consuming, and not sufficiently sensitive. In this study impression cytology techniques were evaluated to analyse their diagnostic potential in viral infections of the ocular surface. METHOD: A Biopore membrane device instead of the original impression cytology technique was used to allow better quality and handling of the specimens. The impressions were processed, using monoclonal antibodies and immunoperoxidase or immunofluorescence techniques to assess the presence of herpes simplex virus, varicella zoster virus, or adenovirus antigens. Ocular surface specimens from healthy individuals (n = 10) and from patients with suspected viral surface disease (n = 19) were studied. Infected and non-infected cell cultures served as controls. RESULTS: This modified technique of impression cytology allowed the collection of large conjunctival and corneal epithelial cell layers with excellent morphology. Immunocytological staining of these samples provided diagnostic results for all three viruses in patients with viral surface disease. CONCLUSIONS: The use of Biopore membrane devices for the collection of ocular surface epithelia offers new diagnostic possibilities for external eye diseases. Immunopathological methods that are applied directly on these membrane devices can provide virological results within 1-4 hours. This contributes considerably to the clinical management of patients with infectious diseases of the ocular surface.

Antigens, Viral↗