aspergillosis/hypoxia

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Reducing hypoxia and inflammation during invasive pulmonary aspergillosis by targeting the Interleukin-1 receptor.

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Hypoxia as a result of pulmonary tissue damage due to unresolved inflammation during invasive pulmonary aspergillosis (IPA) is associated with a poor outcome. Aspergillus fumigatus can exploit the hypoxic microenvironment in the lung, but the inflammatory response required for fungal clearance can

In vivo hypoxia and a fungal alcohol dehydrogenase influence the pathogenesis of invasive pulmonary aspergillosis.

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Currently, our knowledge of how pathogenic fungi grow in mammalian host environments is limited. Using a chemotherapeutic murine model of invasive pulmonary aspergillosis (IPA) and (1)H-NMR metabolomics, we detected ethanol in the lungs of mice infected with Aspergillus fumigatus. This result

Hypoxia Decreases Diagnostic Biomarkers for Aspergillosis In Vitro.

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The aim of the study was to evaluate the influence of hypoxia on galactomannan and (1,3)-β-d-glucan release of clinically relevant Aspergilli in vitro. Hypoxia decreased biomass and consequently led to lower biomarker release. However, when normalized to biomass, hypoxia led to increased

Acute fulminant invasive pulmonary aspergillosis in an immunocompetent host: An autopsy case report.

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A 62-year-old previously healthy male who was a welder/smoker/drinker was admitted to Kani Tono Hospital for severe hypoxemia (Day 0). Initial physical and radiological examinations suggested an acute exacerbation of chronic obstructive pulmonary disease. However, respiratory failure developed

Pulmonary aspergillosis causing right ventricular failure and ascites in meat-type chickens.

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Experimentally induced pulmonary aspergillosis in one-day-old chicks resulted in some with no clinical signs or little damage while others developed marked interstitial pneumonia. Chicks with severe lung damage died from respiratory failure (60%) or developed pulmonary hypertension followed by right

Resolution of secondary pulmonary alveolar proteinosis following treatment of rhinocerebral aspergillosis.

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Pulmonary alveolar proteinosis can be secondary to inhaled dust exposure, malignancy, and chronic pulmonary infections. However, pulmonary alveolar proteinosis secondary to extrapulmonary aspergillosis has never been reported. We report herein a case of pulmonary alveolar proteinosis secondary to

Case of pseudomembranous necrotizing tracheobronchial aspergillosis in an immunocompetent host.

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A 44-year-old Korean male died of rapidly progressive respiratory failure and refractory hypoxemia in 8 days after being admitted with a fever and dyspnea. The patient was diagnosed with pseudomembranous necrotizing tracheobronchial aspergillosis by fibroptic bronchoscopy and it was not related to

Implications of hypoxic microenvironments during invasive aspergillosis.

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In order to cause disease, all pathogens must tolerate microenvironmental stresses encountered in vivo during infection. One microenvironmental stress that is known to occur at sites of tissue damage is hypoxia. Yet, the occurrence and impact of hypoxic microenvironments during invasive

Invasive Aspergillosis After Non-Fatal Drowning.

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Pneumonitis and pneumonia after non-fatal drowning are common and the pathogens involved are numerous. However, invasive aspergillosis after non-fatal drowning in immunocompetent individuals is relatively rare. Here, we report a case of invasive aspergillosis complicated by pulmonary

Eosinophilic Granulomatosis with Polyangiitis preceding allergic bronchopulmonary aspergillosis.

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A 61-year-old Chinese man with long-standing, stable Eosinophilic Granulomatosis with Polyangiitis (EGPA) and asthma, presented with acute hypoxemia and declining obstructive pulmonary function. Elevated serum IgE levels, positive Aspergillus fumigatus specific IgE and CT findings of central

Invasive pulmonary aspergillosis resulting in respiratory failure during neutrophil recovery from postchemotherapy neutropenia in three patients with acute leukaemia.

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Respiratory failure is a severe complication of invasive pulmonary aspergillosis (IPA). Its pathogenesis is not well understood. We herein describe three cases of subacute respiratory failure that occurred during the recovery phase of neutropenia following induction chemotherapy for acute leukaemia

[A case of chronic myelogenous leukemia with pulmonary aspergillosis diagnosed by the detection of circulating Aspergillus antigen].

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Immunocompromised hosts usually develop invasive mycotic disease. Among many pathogenic fungi. Aspergillus spp, is the most common pathogen of respiratory infection. Early diagnosis of invasive type pulmonary aspergillosis is still difficult, and the treatment is usually difficult. Many

Proangiogenic growth factors potentiate in situ angiogenesis and enhance antifungal drug activity in murine invasive aspergillosis.

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In invasive pulmonary aspergillosis, direct invasion and occlusion of pulmonary vasculature by Aspergillus hyphae causes tissue hypoxia, which is enhanced by secreted fungal metabolites that downregulate compensatory angiogenic signaling pathways. We assessed the effects of basic fibroblast growth

Successful long-term extracorporeal membrane oxygenation for invasive pulmonary aspergillosis: a case report.

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BACKGROUND Extracorporeal membrane oxygenation is an established life-saving procedure for severe acute respiratory failure due to various causes. In general, the duration of extracorporeal membrane oxygenation ranges from 1 to 2 weeks, with withdrawal recommended if no improvement is noted. We

In vivo bioluminescence imaging and histopathopathologic analysis reveal distinct roles for resident and recruited immune effector cells in defense against invasive aspergillosis.

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BACKGROUND Invasive aspergillosis (IA) is a major cause of infectious morbidity and mortality in immune compromised patients. Studies on the pathogenesis of IA have been limited by the difficulty to monitor disease progression in real-time. For real-time monitoring of the infection, we recently

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Herbal & Natural Medicine

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