APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
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The main goal of this study was to develop a vaccination strategy that would enhance the protective response against the recombinant type A flagellin (r-fla-A) of Pseudomonas aeruginosa in the burn wound sepsis model. Inbred mice were immunized with r-fla-A with or without alum adjuvant. The vaccinated mice were burned and challenged with P. aeruginosa. ⋯ Anti r-fla-A antibody promoted phagocytosis of the PAK strain, and the number of viable bacterial cells decreased over 53.1%; In contrast, low opsonophagocytic killing activity (17.4%) was observed when the antiserum to r-fla-A was treated with the PAO1 strain. The anti r-fla-A antisera was able to inhibit the motility of the homologous strains; however, they did not inhibit the heterologous strains. We concluded that active immunization with recombinant type A-flagellin could protect burn mice against lethal P. aeruginosa challenge via immobilization of the pathogen which promoted the phagocytic activity.
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Alexander disease (AxD) is a neurodegenerative disorder with prominent white matter degeneration and the presence of Rosenthal fibers containing aggregates of glial fibrillary acidic protein (GFAP), and small stress proteins HSP27 and αB-crystallin, and widespread reactive gliosis. AxD is caused by mutations in GFAP, the main astrocyte intermediate filament protein. We previously showed that intermediate filament protein synemin is upregulated in reactive astrocytes after neurotrauma. ⋯ Many of the GFAP-positive reactive astrocytes were positive for synemin, and synemin was also present in Rosenthal fibers. We show that synemin is expressed in reactive astrocytes in AxD, and is also present in Rosenthal fibers. The potential role of synemin in AxD pathogenesis remains to be investigated.
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The aim of this work was to study the vascular endothelial growth factor A (VEGF-A) pathway and peritumoral brain edema (PTBE) through comparison of non-angiomatous and angiomatous meningiomas. Meningiomas are common intracranial tumors, which often have PTBE. VEGF-A is an integral part of PTBE formation and angiogenesis, and the capillary-rich angiomatous meningiomas are known for their PTBE. ⋯ Neuropilin-1 protein levels were lower in angiomatous meningiomas (p < 0.0001). The VEGF-A pathway and tumor capillary length may be essential for PTBE-formation in meningiomas. Further investigations of this pathway could lead to earlier therapy and targeted pharmacological treatment options.
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Studies on gastrointestinal stromal tumors (GISTs) in young patients are limited due to their rarity, and none have been conducted in Asian populations. GISTs from patients under the age of 30 were retrospectively reviewed and were analyzed for clinicopathologic features, immunohistochemistry for SDHB (succinate dehydrogenase subunit B), and mutations for exon 9, 11, 13, and 17 of KIT gene and exon 12, 14, and 18 of PDGFRA gene. We found two pediatric (<18 years old) and 20 young adult (18-30 years old) GIST cases. ⋯ In summary, compared with pediatric GIST cases, young adult GISTs are heterogeneous and share the characteristics of both pediatric and adult GISTs. When a mesenchymal tumor is clinically suspected in the small intestine of young adults, a GIST should be included in the differential diagnoses. Further mutation studies and extensive treatments are recommended for these cases.
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Our recent non-biased proteomic screening study revealed elevated SerpinA1 i.e. alpha-1-antitrypsin (AAT) levels in induced sputum of smokers with Chronic obstructive pulmonary disease (COPD). This study was designed to further investigate the role of AAT in smokers and subjects with COPD. The expression/distribution of AAT was studied by immunohistochemistry/digital image morphometry in the lung, by Western blot in the lung and sputum, and by ELISA in the plasma at baseline (n = 349) and after a 2-year follow-up (n = 58). ⋯ Plasma AAT levels were elevated in smokers with/without COPD compared with non-smokers. In the follow-up, plasma AAT concentrations decreased significantly after quitting smoking. Chronic smoking/COPD leads to AAT elevation especially in the endothelium of the lung periphery; these changes reflect only modestly to the AAT in sputum, while plasma AAT significantly reflects smoking-related systemic manifestations, and decreases after smoking cessation.