1,763 research outputs found
Environmental isolation of black yeast-like fungi involved in human infection
The present study focuses on potential agents of chromoblastomycosis and
other endemic diseases in the state of Paraná, Southern Brazil. Using a
highly selective protocol for chaetothyrialean black yeasts and relatives,
environmental samples from the living area of symptomatic patients were
analysed. Additional strains were isolated from creosote-treated wood and
hydrocarbon-polluted environments, as such polluted sites have been supposed
to enhance black yeast prevalence. Isolates showed morphologies compatible
with the traditional etiological agents of chromoblastomycosis, e.g.
Fonsecaea pedrosoi and Phialophora verrucosa, and of agents of
subcutaneous or systemic infections like Cladophialophora bantiana
and Exophiala jeanselmei. Some agents of mild disease were indeed
encountered. However, molecular analysis proved that most environmental
strains differed from known etiologic agents of pronounced disease syndromes:
they belonged to the same order, but mostly were undescribed species. Agents
of chromoblastomycosis and systemic disease thus far are prevalent on the
human host. The hydrocarbon-polluted environments yielded yet another spectrum
of chaetothyrialean fungi. These observations are of great relevance because
they allow us to distinguish between categories of opportunists, indicating
possible differences in pathogenicity and virulence
Mice Deficient in Endothelial α5 Integrin are Profoundly Resistant to Experimental Ischemic Stroke
Stroke is a disease in dire need of better therapies. We have previously shown that a fragment of the extracellular matrix proteoglycan, perlecan, has beneficial effects following cerebral ischemia via the α5β1 integrin receptor. We now report that endothelial cell selective α5 integrin deficient mice (α5 KO) are profoundly resistant to ischemic infarct after transient middle cerebral artery occlusion. Specifically, α5 KOs had little to no infarct 2–3 days post-stroke, whereas controls had an increase in mean infarct volume over the same time period as expected. Functional outcome is also improved in the α5 KOs compared with controls. Importantly, no differences in cerebrovascular anatomy or collateral blood flow were noted that could account for this difference in ischemic injury. Rather, we demonstrate that α5 KOs have increased blood-brain barrier integrity (increased expression of claudin-5, and absent brain parenchymal IgG extravasation) after stroke compared with controls, which could explain their resistance to ischemic injury. Additionally, inhibition of α5 integrin in vitro leads to decreased permeability of brain endothelial cells following oxygen-glucose deprivation. Together, these findings indicate endothelial cell α5 integrin plays an important role in stroke outcome and blood-brain barrier integrity, suggesting that α5 integrin could be a novel therapeutic target for stroke
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