| DB ID | MyCo_1626 |
| Title | Hypoxia promotes danger-mediated inflammation via receptor for advanced glycation end products in cystic fibrosis |
| Year | 2013 |
| PMID | 24127697 |
| Fungal Diseases involved | Fungal Pneumonia |
| Associated Medical Condition | Hypoxia and Cystic Fibrosis |
| Genus | Aspergillus |
| Species | fumigatus |
| Organism | Aspergillus fumigatus |
| Ethical Statement | Experiments were performed according to the Italian Approved Animal Welfare Assurance 245–2011-B. |
| Site of Infection | Lungs |
| Opportunistic invasive | Opportunistic |
| Sample type | Body fluid |
| Sample source | Bronchoalveolar lavage fluid (BALF) |
| Host Group | Human |
| Host Common name | Human |
| Host Scientific name | Homo sapiens |
| Biomarker Name | HMGB1 |
| Biomarker Full Name | High mobility group box 1 |
| Biomarker Type | Diagnostic |
| Biomolecule | Protein |
| Geographical Location | Italy |
| Cohort | Human bronchial epithelial (HBE) cells homozygous for the dF508 mutation were obtained from lung transplants (patients with CF) or lung resections (patients without CF) and cultured. A prospective multicenter longitudinal genetic association study involving 277 patients of Caucasian origin who had a proven diagnosis of CF (CFTR genotyping, sweat testing, and clinical phenotype) was performed. Clinical records from each patient were reviewed and clinical data including age, gender, lung function testing, measures of nutrition, microbiological findings and vital status were abstracted. Study approval was obtained from institutional review boards at each site and written informed consent was obtained from the participants, or, in case of minors, from parents or guardian. |
| Cohort No. | 277 |
| Age Group | None |
| P Value | None |
| Sensitivity | None |
| Specificity | None |
| Positive Predictive Value | None |
| MIC | None |
| Fold Change | None |
| Pathway | None |
| Disease Introduction Mechanism | In patients with cystic fibrosis (CF), lung disease is the major cause of morbidity and mortality. The progressive decline of pulmonary function is caused by a vicious cycle of airways infection and inflammation. The pulmonary immune response in CF is characterized by an early and nonresolving activation of the innate immune system, which is dysregulated at several levels, does not result in enhanced bacterial clearance, and plays a pivotal role in the pathogenesis of lung disease in CF. This is supported by several studies that have documented an altered balance of inflammatory and antiinflammatory cytokines in CF, such that targeting specific inflammatory and anti-inflammatory pathways may represent a valid therapeutic strategy in CF. |
| Technique | ELISA |
| Analysis Method | ELISA Based |
| ELISA kits | Quantikine Human RAGE Immunoassay kit (R&D Systems, Minneapolis, MN), ELISA, human S100B ELISA KIT (Millipore, Billerica, MA) |
| Assay Data | None |
| Validation Techniques used | ELISA, Hypoxyprobe Treatment, Western Blotting, Immunohistochemistry, RT-PCR |
| Up Regulation Down Regulation | UP regulated |
| Sequence Data | S100B - Human (GenBank: M59486) and murine (GenBank: NC_000076.5) |
| External Link | None |
