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1.
Cornea ; 34(12): 1560-3, 2015 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-26398157

RESUMO

PURPOSE: Fuchs flecks (FFs) have been previously identified at the leading edge of pterygia and may represent collections of epithelial stem-like cells that give rise to this condition. This study aims to evaluate the clinical significance of FFs in patients with ocular surface disorders, such as pterygium and pinguecula, by in vivo confocal microscopy (IVCM). METHODS: This study is a Single-center, retrospective, observational case series of 40 eyes from 20 patients with clinical diagnoses of pinguecula or pterygium, or both. IVCM (Rostock Cornea Module; Heidelberg Engineering, Heidelberg, Germany) was performed on patients with pinguecula or pterygium, or both. The presence of FFs on the ocular surface of patients with pterygium and pinguecula was assessed by IVCM and subsequently documented. RESULTS: FFs were present in 24 of 30 eyes (80.0%) in paired macroscopically normal nasal or limbal regions, 19 of 20 (95.0%) in pinguecula, 13 of 15 (86.7%) in primary pterygia, and 7 of 7 (100%) in recurrent pterygia. CONCLUSIONS: High rates of FFs were identified at the head of pinguecula, primary pterygium, recurrent pterygium, and macroscopically normal nasal and temporal limbus. We postulate that FFs may represent precursor lesions to UV-associated ocular surface pathology. Identification of Fuchs fleck by IVCM may permit clinicians to predict the patients who may progress to develop more advanced pathology.


Assuntos
Túnica Conjuntiva/efeitos da radiação , Limbo da Córnea/patologia , Pinguécula/diagnóstico , Pterígio/diagnóstico , Lesões por Radiação/diagnóstico , Células-Tronco/patologia , Raios Ultravioleta/efeitos adversos , Adulto , Idoso , Feminino , Humanos , Masculino , Microscopia Confocal , Pessoa de Meia-Idade , Pinguécula/etiologia , Pterígio/etiologia , Lesões por Radiação/etiologia , Estudos Retrospectivos
2.
Respir Med ; 106(5): 701-9, 2012 May.
Artigo em Inglês | MEDLINE | ID: mdl-22349068

RESUMO

BACKGROUND: Potential antigens inducing sarcoid inflammation include mycobacterial and auto-antigens. Paradoxically, peripheral anergy to common recall antigens also occurs, possibly due to impaired dendritic cell or regulatory T-cell responses, or impaired T-cell co-stimulation. The purpose of this study was to compare peripheral blood responses of patients with sarcoidosis to candidate antigens, and examine CD28 T-cell co-stimulation. METHODS: Peripheral blood mononuclear cell (PBMC) responses were examined from patients with sarcoidosis (n=16) and healthy control subjects (n=22) following PBMC stimulation with: anti-CD3/CD28 coated beads; Mycobacterium tuberculosis ESAT-6 and KatG peptides; vimentin and lysyl tRNA peptides; and common recall antigens, including cytomegalovirus (CMV) cell lysate as well as CMV, Epstein-Barr virus, influenza virus (CEF) peptides. RESULTS: ESAT-6/KatG peptide stimulation induced greater numbers of IFN-γ producing T-cells, and elevated IL-2, IL-6 and TNF-α production in sarcoidosis compared to purified protein derivative (PPD)-negative healthy control subjects. PBMCs from patients with sarcoidosis showed reduced IFN-γ producing T-cells following stimulation with CMV lysate, CEF peptides and CD3/CD28 beads; and reduced IL-4 and TNF-α production following CD3/CD28 activation. CONCLUSIONS: Patients with sarcoidosis exhibit greater PBMC responses to M. tuberculosis antigens compared to PPD-negative controls, but reduced T-cell responses to common recall antigens. One contributing mechanism may be impairment of T-cell CD28 co-stimulation.


Assuntos
Antígenos CD28/imunologia , Leucócitos Mononucleares/imunologia , Sarcoidose/imunologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Antígenos de Bactérias/imunologia , Autoantígenos/imunologia , Células Cultivadas , Anergia Clonal/imunologia , Citocinas/biossíntese , Feminino , Volume Expiratório Forçado/fisiologia , Humanos , Interferon gama/biossíntese , Ativação Linfocitária/imunologia , Masculino , Pessoa de Meia-Idade , Mycobacterium tuberculosis/imunologia , Sarcoidose/fisiopatologia , Subpopulações de Linfócitos T/imunologia , Capacidade Vital/fisiologia , Adulto Jovem
3.
Cornea ; 30(7): 835-7, 2011 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-21389852

RESUMO

PURPOSE: To report a patient who developed a crystalline keratopathy after bluebottle envenomation of the cornea. METHOD: Case report with histopathological correlation and literature review. RESULTS: A 61-year-old man presented to the Ophthalmology clinic after he was stung in the left eye by a bluebottle while swimming in the sea. He complained of ocular and facial pain, facial swelling, and transient blurred vision. First aid by the beach included a hot shower and methoxyflurane for the pain. Crystalline deposits and pseudodendritiform epithelial defects were noted on slit-lamp examination. Topical chloramphenicol was prescribed, and 2 days after the injury, the cornea was debrided of persisting crystalline material. The cornea healed quickly after debridement with visual acuity improving from 6/9 to 6/6 in the affected eye. Microscopic examination demonstrated the corneal crystals to be irregularly shaped and nonrefractile with squared off edges. Raman spectroscopy partially identified the crystals as calcium based. CONCLUSIONS: Although bluebottle stings of the cornea are infrequent, they may be challenging to manage. In addition to inactivation of the nematocysts and pain management, early debridement of the foreign matter may aid in the rapid resolution of the symptoms.


Assuntos
Mordeduras e Picadas/etiologia , Cálcio , Venenos de Cnidários/efeitos adversos , Doenças da Córnea/etiologia , Hidrozoários , Corpos de Inclusão/patologia , Animais , Mordeduras e Picadas/patologia , Mordeduras e Picadas/terapia , Cloranfenicol/uso terapêutico , Terapia Combinada , Doenças da Córnea/patologia , Doenças da Córnea/terapia , Desbridamento , Dor Ocular/etiologia , Humanos , Masculino , Pessoa de Meia-Idade , Acuidade Visual
4.
Invest Ophthalmol Vis Sci ; 51(5): 2558-67, 2010 May.
Artigo em Inglês | MEDLINE | ID: mdl-20019359

RESUMO

PURPOSE: Ocular pigment epithelial cells are hypothesized to play a role in the pathogenesis of acute anterior uveitis (AAU), where LPS activation of Toll-like receptors (TLRs) may serve as a trigger. In this study, the expression of LPS receptors in iris pigment epithelium (IPE) was determined. METHODS: RT-PCR, flow cytometry, Western blot, and immunohistochemistry were used to investigate the expression of the LPS receptor complex (TLR4, MD-2, and CD14) in primary human IPE. Cytokine secretion by LPS-treated IPE was measured by multiplex bead array and ELISA. The role of CD14 in modulating the LPS response was investigated by addition of soluble CD14 and by antibody neutralization studies. In vivo expression of CD14 was examined by immunohistochemistry and Western blot analysis. RESULTS: IPE expressed TLR4, MD-2, and CD14 in vitro and secreted a panel of proinflammatory cytokines (IL-6, CXCL8, CXCL10, CCL2, CCL4, and CCL5) when stimulated with LPS. CXCL8 secretion by LPS-treated IPE was dependent on CD14 and TLR4. CD14 was detected in CD68+ cells in the iris by immunohistochemistry and in normal aqueous by Western blot analysis. CONCLUSIONS: IPE cells express a functional LPS receptor complex and are capable of promoting ocular inflammation through secretion of an array of proinflammatory mediators. CD14 was identified as a key molecule that modulated the LPS response in IPE.


Assuntos
Iris/metabolismo , Receptores de Lipopolissacarídeos/genética , Epitélio Pigmentado Ocular/metabolismo , Humor Aquoso/metabolismo , Western Blotting , Técnicas de Cultura de Células , Primers do DNA , Ensaio de Imunoadsorção Enzimática , Citometria de Fluxo , Expressão Gênica/efeitos dos fármacos , Humanos , Iris/citologia , Receptores de Lipopolissacarídeos/metabolismo , Lipopolissacarídeos/farmacologia , Antígeno 96 de Linfócito/genética , Antígeno 96 de Linfócito/metabolismo , Epitélio Pigmentado da Retina/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Receptor 2 Toll-Like/genética , Receptor 2 Toll-Like/metabolismo , Receptor 4 Toll-Like/genética , Receptor 4 Toll-Like/metabolismo , Úvea/metabolismo
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