3 research outputs found

    Polluted Air Exposure Compromises Corneal Immunity and Exacerbates Inflammation in Acute Herpes Simplex Keratitis

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    Air pollution is a serious environmental issue worldwide in developing countries?megacities, affecting the population?s health, including the ocular surface, bypredisposing or exacerbating other ocular diseases. Herpes simplex keratitis (HSK) iscaused by the herpes simplex virus type 1 (HSV-1). The primary or recurring infection inthe ocular site causes progressive corneal scarring that may result in visual impairment.The present study was designed to study the immunopathological changes of acute HSKunder urban polluted air, using the acute HSK model combined with an experimentalurban polluted air exposure from Buenos Aires City. We evaluated the corneal clinicaloutcomes, viral DNA and pro-inflammatory cytokines by RT-PCR and ELISA assays,respectively. Then, we determined the innate and adaptive immune responses in bothcornea and local lymph nodes after HSV-1 corneal by immunofluorescence staining andflow cytometry. Our results showed that mice exposed to polluted air develop a severeform of HSK with increased corneal opacity, neovascularization, HSV-1 DNA andproduction of TNF-a, IL-1b, IFN-g, and CCL2. A high number of corneal residentimmune cells, including activated dendritic cells, was observed in mice exposed topolluted 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 apredominant Th1 type T cell response over Tregs in local lymph nodes during acute HSKwith decreased corneal Tregs. These findings provide strong evidence that urban pollutedair might trigger a local imbalance of innate and adaptive immune responses thatexacerbate HSK severity. Taking this study into account, urban air pollution should beconsidered a key factor in developing ocular inflammatory diseases.Fil: Sendra, Victor German. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Tau, Julia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Zapata, Gustavo Leonardo. Universidad de Buenos Aires; ArgentinaFil: Lasagni Vitar, Romina Mayra. Universidad de Buenos Aires; ArgentinaFil: Illian, Eduardo. Dirección Nacional de Instituto de Investigación.Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán"; ArgentinaFil: Chiaradía, Pablo. Universidad de Buenos Aires; ArgentinaFil: Berra, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentin

    The First Argentinian Family with Familial Amyloidosis of the Finnish Type

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    Familial amyloidosis of the Finnish type or Meretoja syndrome is a rare autosomic dominant inherited systemic condition. It was first described by Meretoja in Finland in 1969. It is a disease produced by a single mutation in the gene coding for gelsolin, which generates an abnormal protein that cumulates in tissues and leads to various signs. Obtaining an early diagnosis can be challenging, as the first manifestations of the disease are ophthalmological and may only be seen with slit-lamp biomicroscopy. We present the first 3 cases diagnosed in Argentina, confirmed by genetic molecular testing
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