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Copyright of Arquivos Brasileiros de Oftalmologia is the property of Arquivos Brasileiros de Oftalmologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Air pollution is a serious environmental issue worldwide in developing countries' megacities, affecting the population's health, including the ocular surface, by predisposing or exacerbating other ocular diseases. Herpes simplex keratitis (HSK) is caused by the herpes simplex virus type 1 (HSV-1). The primary or recurring infection in the ocular site causes progressive corneal scarring that may result in visual impairment. The present study was designed to study the immunopathological changes of acute HSK under urban polluted air, using the acute HSK model combined with an experimental urban polluted air exposure from Buenos Aires City. We evaluated the corneal clinical outcomes, viral DNA and pro-inflammatory cytokines by RT-PCR and ELISA assays, respectively. Then, we determined the innate and adaptive immune responses in both cornea and local lymph nodes after HSV-1 corneal by immunofluorescence staining and flow cytometry. Our results showed that mice exposed to polluted air develop a severe form of HSK with increased corneal opacity, neovascularization, HSV-1 DNA and production of TNF-α, IL-1β, IFN-γ, and CCL2. A high number of corneal resident immune cells, including activated dendritic cells, was observed in mice exposed to polluted air; with a further significant influx of bone marrow-derived cells including GR1+ cells (neutrophils and inflammatory monocytes), CD11c+ cells (dendritic cells), and CD3+ (T cells) during acute corneal HSK. Moreover, mice exposed to polluted air showed a predominant Th1 type T cell response over Tregs in local lymph nodes during acute HSK with decreased corneal Tregs. These findings provide strong evidence that urban polluted air might trigger a local imbalance of innate and adaptive immune responses that exacerbate HSK severity. Taking this study into account, urban air pollution should be considered a key factor in developing ocular inflammatory diseases. [ABSTRACT FROM AUTHOR]

Objective: To test the feasibility of conducting a full-scale project evaluating the potential value of the phosphorylated neurofilament H (pNF-H) and several cytokines as disability markers in relapsing-remitting multiple sclerosis (RRMS). Methods: Twenty-four patients with 5-year RRMS evolution and eleven healthy control subjects entered the study. None of the participants had an inflammatory systemic or metabolic disease. Disability progression was evaluated using the Expanded Disability Status Scale. Serum level of pNF-H, the anti-inflammatory cytokine transforming growth factor-β 1 (TGF-β1), and the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-17A (IL-17A), monocyte chemotactic protein-1 (MCP-1), and soluble intercellular cell-adhesion molecule 1 (sICAM-1) were quantified using enzyme-linked immunosorbent assay (ELISA). Results: The patients had higher serum level of TGF-β1, IL-6, sICAM-1, and pNF-H. Based on these findings, a sample of at least 49 controls and 89 recent-onset RRMS patients is required to find an at least 1-point between-group difference in pNF-H with a power of 80% and an α error = 0.05. The progression of the disease was correlated with the level of pNF-H (Spearman rho = 0.624, p = 0.006), but not with the cytokines'. Conclusions: The serum level of pNF-H, EDSS score-correlated, might stand for a potential biomarker of disability in RRMS reflecting progressive axonal damage and cumulative neurological deterioration. The novelty of these results warrants conducting a larger confirmatory trial. [ABSTRACT FROM AUTHOR]

Copyright of Arquivos Brasileiros de Oftalmologia is the property of Arquivos Brasileiros de Oftalmologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Purpose: To examine the effects of n-3 and n-6 polyunsaturated fatty acids (n-3 and n-6 PUFAs) in a murine model of herpetic chorioretinitis.Methods: BALB/c mice were fed on three high fat diets, which contained: Menhaden oil (rich in n-3 PUFAs); Safflower oil (rich in n-6 PUFAs); or Corn oil (rich in saturated fatty acids) as control group, 14 days previously and until 12 days following anterior chamber (AC) HSV-1 inoculation.Results: Mice fed on Menhaden oil present an early development of contralateral chorioretinitis by day 6 post-AC HSV-1 inoculation and also significant increase of RNA HSV-1 expression compared with Safflower and Corn oil groups. Furthermore, mice fed on Menhaden oil showed a significant decrease secretion of TNF-α, IFN-γ, IL-2 and IL-10 in splenic cells and both retinas.Conclusion: Our results showed that mice fed on Menhaden oil (n-3 PUFAs) presented an early development of contralateral chorioretinitis by day 6 post-AC HSV-1 inoculation and also a significant increase in RNA HSV-1 expression compared with animals fed on Safflower and Corn oils. This increase of HSV-1 could be associated with the higher development of chorioretinitis. [ABSTRACT FROM AUTHOR]

Copyright of Arquivos Brasileiros de Oftalmologia is the property of Arquivos Brasileiros de Oftalmologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Purpose: To evaluate and compare the efficacy of rapamycin used topically in a mouse model of herpetic stromal keratitis. Methods: The corneas were infected with herpes simplex virus type-1 strain KOS. Animals were divided into: control (CG), rapamycin (RAPA), cyclosporine (CsA), and dexamethasone (DEXA). The evolution of the disease was assessed clinically and histologically. Results: On day 10 postinfection (pi), the RAPA group showed only a significantly lower angiogenic development than the CG. On day 14 pi, the treated groups had significantly lower scores for angiogenesis and necrosis than the CG. Also, on day 14 pi, the RAPA and DEXA groups showed significantly lower histopathological scores compared to the CG. Conclusions: The topical application of 0.05% rapamycin showed greater efficacy than 0.5% cyclosporine and similar efficacy to 0.1% dexamethasone to minimize the immuno-inflammatory process. Also, rapamycin showed early inhibition of the formation of new vessels. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the cytotoxicity of a new Latanoprost Benzalkonium chloride (BAK)‐free nanoemulsion and to compare it with a Latanoprost solution containing BAK. Methods: Normal Human Conjunctival epithelial cells (IOBA‐NHC) were incubated for 15, 30, and 60 minutes with 1:6 dilutions of either latanoprost solution containing BAK (LSc), (latanoprost 0.005%, BAK 0.02%, Xalatan, Pfizer) or latanoprost nanoemulsion (LNe), (latanoprost 0.005%, potassium sorbate 0.18%; Louten Emulsion, POEN). Cytotoxicity was determined by MTT assay. Cell death was measured by flow cytometry using annexin V‐FITC and propidium iodide. Results: Cytotoxicity evaluation: the values of cell viability and proliferation obtained from cells exposed to LNe were between 80 and 90% relative to control group, whereas values obtained from cells exposed to LSc were around 30% relative to control group at all study times (p < 0.05 at 15 and 30 minutes; p < 0.01 at 60 minutes). Cell death evaluation: the percentage of viability was significantly lower in cells exposed to LSc compared with those incubated with LNe at all study times (p < 0.05 at 15 and 30 minutes; p < 0.01 at 60 minutes). Viability of cells exposed to LNe was higher than 90% at all study times, whereas there was a time‐dependent decrease in cells exposed to Lsc. The percentage of viable cells in the LNe group was comparable to the viability of control group (93.1%) at all study times. No statistical differences between groups reached in early apoptotic cells. A significant increase of late apoptosis and necrosis cells were observed at all study times for those incubated with Lsc (p < 0.05; p < 0.01 at 30 and 60 minutes). Conclusions: The new latanoprost nanoemulsion is significantly less cytotoxic on human conjunctival cells than LSc. It suggests that the new formulation could be gentler on the eye surface than currently available BAK preserved latanoprost solutions, with levels of cytotoxicity equivalent to control. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the concentration of tear lysozyme in individuals with Sjogren´s syndrome, meibomian gland dysfunction, and non-dry-eye disease., Methods: Ninety subjects were recruited for this study, including 30 with Sjogren´s syndrome, 30 with meibomian gland dysfunction, and 30 with non-dry-eye disease. All subjects were referred to participate in the study based on a "dry eye" investigation. They underwent a complete ocular surface ophthalmic examination encompassing ocular surface disease index, biomicroscopy, tear break-up time, Schirmer test type I, conjunctival vital staining with fluorescein and lissamine green, tear lysozyme concentration, and impression cytology., Results: Clinical tests yielded the following results: ocular surface disease index Sjogren´s syndrome: 64.5 ± 22.6 meibomian gland dysfunction: 43.5 ± 21.4, non-dry-eye disease: 6.7 ± 4.3 (p=0.02 between groups); Schirmer I test (mm/5 min): Sjogren´s syndrome: 4.95 ± 2.25, meibomian gland dysfunction: 13.28 ± 1.53, non-dry-eye disease 13.70 ± 1.39 (p<0.01 Sjogren´s syndrome vs. non-dry-eye disease and p<0.01 meibomian gland dysfunction vs. non-dry-eye disease); tear break-up time (seconds): Sjogren´s syndrome: 3.97 ± 1.47, meibomian gland dysfunction: 3.95 ± 0.86, non-dry-eye disease: 7.25 ± 1.90 (p<0.01 Sjogren´s syndrome vs. non-dry-eye disease and p<0.01 meibomian gland dysfunction vs. non-dry-eye disease); Lissamine green score: Sjogren´s syndrome-dry-eye: 6.18 ± 2.14, meibomian gland dysfunction-dry-eye: 5.27 ± 1.27, non-dry-eye disease: 1.52 ± 0.97 (p<0.01 Sjogren´s syndrome vs. non-dry-eye disease and p<0.01 meibomian gland dysfunction vs. non-dry-eye disease); impression cytology score: Sjogren´s syndrome: 1.88 ± 0.92, meibomian gland dysfunction: 1.67 ± 0.56, non-dry-eye: 0.45 ± 0.44 (p<0.01 Sjogren´s syndrome vs. non-dry-eye disease and p<0.01 meibomian gland dysfunction vs. non-dry-eye disease) and; tear lysozyme concentration (µg/mL): Sjogren´s syndrome: 751.25 ± 244.73, meibomian gland dysfunction: 1423.67 ± 182.75, non-dry-eye disease: 1409.90 ± 188.21 (p<0.01 Sjogren´s syndrome vs. non-dry-eye disease and p<0.01 Sjogren´s syndrome vs. meibomian gland dysfunction)., Conclusion: The concentration of lysozyme in the tears was lower in Sjögren's syndrome patients than in meibomian gland dysfunction and non-dry-eye disease groups. Hence, the lacrimal lysozyme could be considered as a simple, non-invasive, and economical biomarker to differentiate between Sjögren's syndrome dry eye disease and meibomian gland dysfunction dry eye disease.

Studies on the inflammatory burden in recent-onset psoriatic arthritis (PsA) patients without conventional cardiovascular risk factors (CVRFs) are not available. This preliminary study focuses on cardiovascular risk in cutaneous psoriasis (CPs) and recent-onset PsA patients. Blood biochemistry (glucose, cholesterol, uric acid, lipid profile and apolipoprotein B) was analyzed using standard kits. Proatherogenic inflammation markers, C-reactive protein (CRP) and interleukin-6 (IL-6), and endothelial activators monocyte chemoattractant protein-1 (MCP-1) and soluble intercellular adhesion molecule-1 (sICAM-1), were determined by enzyme-linked immunosorbent assay. Ultrasound images allowed measuring carotid intima-media thickness (cIMT). Our study first shows an increase in cIMT, and in serum levels of sICAM-1 and CRP in recent-onset PsA patients not presenting conventional CVRFs over the non-medicated time-period, from disease diagnosis to the beginning of pharmacological treatment, compared with healthy subjects. The outcome highlights the importance of monitoring serum level of sICAM1, CRP, and cIMT, and the value of primary prevention in psoriatic patients even with no history of cardiovascular events.

Purpose: The aim of this study was to evaluate oxidative stress markers in human conjunctival epithelial cells (IOBA-NHC) exposed to diesel exhaust particles (DEP)., Methods: Reactive oxygen (ROS) and nitrogen (RNS) species production; hydrogen peroxide (H2O2) levels; protein oxidation; antioxidant enzymes activities (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GPx], glutathione S-transferase [GST], and glutathione reductase [GR]); total reactive antioxidant potential (TRAP); reduced (GSH) and oxidized glutathione (GSSG) were evaluated. Transmission electron microscopy was performed to evaluate DEP uptake., Results: Diesel exhaust particles were entrapped by membrane protrusions developed by IOBA-NHC. Cells exposed to DEP 50 and 100 μg/mL showed a significant increase in ROS, RNS, H2O2 levels, SOD, GPx, and GST compared with the control group. A significant decay in GR was observed in both groups, meanwhile CAT levels remained unchanged. The group exposed to DEP 100 μg/mL displayed a significant increase in protein oxidation. In both groups, TRAP was significantly reduced as well as the GSH/GSSG ratio., Conclusions: The decrease in nonenzymatic antioxidants and the compensatory increase of SOD, GPX, and GST activities are consequence of the increase in ROS and RNS production due to DEP exposure and its accumulation inside the cells. The decay in GR activity leads to the decrease in GSH/GSSG recycling. These results suggest that oxidative stress could play an important role in the development of DEP effects on human conjunctival epithelial cells.

Purpose: To evaluate the effect of diesel exhaust particles (DEP) on the viability, proliferation, apoptosis, secretion of cytokines (IL-6, IL-8, and TNF-α), and mucin gene transcription (MUC1, MUC5AC, and MUC16) in human epithelial cells of the cornea (HCLE) and conjunctiva (IOBA-NHC)., Methods: HCLE and IOBA-NHC cells were incubated with DEP (10-500 μg/mL) for 24 hours. Cell proliferation was evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Apoptotic cells were measured by an annexin V-FITC and propidium iodide kit for flow cytometry. Proinflammatory cytokines were determined by an ELISA kit. Mucin gene transcription was quantified by real-time PCR., Results: DEP significantly decreased the viability, proliferation, and secretion of IL-8, but increased the secretion of IL-6 on both HCLE and IOBA-NHC cell lines in a dose-dependent manner. Neither cornea nor conjunctiva cells incubated with DEP released TNF-α. DEP induced a significant increase in the percentage of apoptotic cells in IOBA-NHC, whereas no changes were observed in HCLE. Finally, DEP significantly decreased the transcription levels of MUC1 and MUC16 in HCLE, but increased the transcription levels of MUC1, MUC5AC, and MUC16 in IOBA-NHC., Conclusions: These findings suggest that human corneal and conjunctival epithelial cells incubated with DEP showed cytotoxicity and an inflammatory response mediated by IL-6, not by TNF-α or IL-8. Also, the decrease in mucin expression in the cornea cells might leave exposed areas in the cornea for contact with DEP. Finally, the increase in mucin expression in the conjunctiva cells might be involved at least in the clearance of DEP to protect the ocular epithelium.

The objective of this report is to describe a case of crystalline keratopathy caused by the Streptococcus mitis group corresponding to a patient who attended hospital for discomfort in her right eye. The ophthalmological examination showed an interrupted stitch of 10-0 nylon suture without tension and with attached mucus secretions. The loose suture was removed under aseptic conditions. Moxifloxacin 0.5 % eye drops were topically indicated. The treated eye successfully epithelialized and evolved favorably. However, after 15 days, a white tree-shaped infiltrate developed. A corneal sample was taken in the operating room, threading the intrastromal path of the removed stitch with a 7-0 vicryl suture. Vancomycin 50 mg/ml drops were indicated. The infiltrate, which was stable for 45 days, later increased its size and tissue necrosis occurred with danger of corneal perforation. A bipedicle conjunctival flap was performed in the affected corneal area, which evolved favorably. After spontaneous conjunctival flap retraction, only corneal scarring and neovascularization outside the visual axis were observed.