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C Tagesson

Publications and source records attributed to C Tagesson.

167 records · Page 10Linked to original sources
PubMedDate not supplied

Demonstration of different forms of the anti-inflammatory proteins lipocortin-1 and Clara cell protein-16 in human nasal and bronchoalveolar lavage fluids.

The anti-inflammatory proteins lipocortin-1 and Clara cell protein-16 (CC-16) were studied in two-dimensional gel electrophoresis (2-DE) protein patterns of human nasal lavage fluids (NLFs) and bronchoalveolar lavage fluids (BALFs). Seven forms of lipocortin-1 were detected with Western immunoblots: three isoforms with an apparently normal Mr of 38 kDa and pI of 5.9, 6.0 and 6.1, and four truncated variants with pI/kDa 6.0/36, 6.4/36, 7.0/33, and 7.4/34. Four 6 kDa isoforms of CC-16 were found with pI 4.6, 4.8, 4.9, and 5.2. Lipocortin-1 and CC-16 were expressed in all individuals tested although not all variants were found in each individual. The overall levels of lipocortin-1 were higher in BALF than NLF and there were significant differences in the distribution of the different lipocortin-1 forms between BALFs and NLFs. One patient with occupational asthma and four children with rhinitis had increased levels of one of the truncated lipocortin-1 forms in NLF (pI/kDa: 7.4/34) and decreased levels of the major CC-16 form (pI/kDa: 4.8/6). The levels of CC-16 but not of lipocortin-1 were higher in BALF from smokers than from nonsmokers. These results indicate that the levels of lipocortin-1 and CC-16 in NLF and BALF may be altered in inflammatory airway disorders. Furthermore, the identification of different forms of the two proteins makes possible more detailed studies on the role of these proteins in inflammatory disease processes and anti-inflammatory therapies.

Annexin A1↗
PubMedDate not supplied

Platelet-activating factor acetylhydrolase activity in intestinal mucosa and plasma of patients with Crohn's disease.

The activity of platelet-activating factor (PAF) acetylhydrolase in biopsy specimens of intestinal mucosa was compared in patients with Crohn's disease (n = 11) and controls (n = 6). In addition, PAF acetylhydrolase activity was determined in the plasma of Crohn patients (n = 30) and healthy subjects (n = 35). The activity of PAF acetylhydrolase in mucosal samples from the distal ileum was significantly lower in Crohn patients than in control patients (p < 0.02), whereas there was no difference in PAF acetylhydrolase activity of colonic or jejunal samples between Crohn patients and controls. The PAF acetylhydrolase activity in the plasma of Crohn patients was significantly decreased as compared to healthy subjects. Crohn patients with high disease activity (symptomatic index > 150) had a significantly lower PAF acetylhydrolase activity in plasma, as compared to patients in clinical remission (symptomatic index < 150; p < 0.02), and as compared to healthy subjects (p < 0.001). PAF acetylhydrolase activity in plasma increased within 4 months after bowel resection (p < 0.05). These findings indicate that the PAF acetylhydrolase activity is decreased in the ileal mucosa of patients with Crohn's disease and that PAF acetylhydrolase activity in plasma is inversely related to disease activity in Crohn's disease. The possibility that PAF acetylhydrolase is one factor of importance for protecting the intestinal mucosa against PAF-mediated inflammation is inferred.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMedDate not supplied

Calcium ionophore-activated neutrophils prestimulated with endotoxin increase pulmonary arterial pressure and vascular leakage in isolated perfused rat lungs: role of platelet-activating factor.

The influence of stimulated polymorphonuclear neutrophils on pulmonary arterial pressure and vascular leakage in isolated perfused rat lungs was investigated. We exposed isolated neutrophils to various stimuli in vitro, instilled the cells in the lung perfusate, and studied the effects on pulmonary arterial pressure and passage of fluorescently labeled dextran (4100 dalton) from the pulmonary circulation into the lung. We found that neutrophils stimulated with the calcium ionophore A23187 or with E. coli endotoxin had no significant influence on the pressure or the passage of dextran. On the other hand, neutrophils preincubated with endotoxin and then stimulated with A23187 caused significant increases, both in pulmonary arterial pressure and accumulation of dextran in the lung. Both these effects were attenuated by BN 52021, a specific platelet-activating factor antagonist, and by nordihydroguaiaretic acid, an agent that inhibited the generation of platelet-activating factor in A23187-stimulated neutrophils. These findings demonstrate that activated neutrophils can increase pulmonary arterial pressure and lung fluid accumulation and suggest that endotoxin-stimulated activated neutrophils exert at least some of their action via generation of platelet-activating factor.

Animals↗