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  • 1
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Eosinophils, mast cells and T lymphocytes are important cells in the allergic inflammatory process. These cells produce and are regulated by cytokines such as interleukin-3 (IL-3), interleukin-5 (IL-5) and granulocyte macrophage-colony stimulating factor (GM-CSF). We initiated this study to evaluate pathological abnormalities and to detect IL-5 in the duodenal mucosa from patients with food allergy.〈section xml:id="abs1-2"〉〈title type="main"〉MethodsEndoscopy duodenal biopsy specimens were obtained from seven food-allergic patients, six atopic healthy controls and six nonatopic healthy controls. IL-5 protein was evaluated by immunohistochemistry. Electron microscopy as well as double immunofluorescent staining were used to identify the labelled cells and to localize IL-5. IL-5 mRNA expression was evaluated by qualitative polymerase chain reaction.〈section xml:id="abs1-3"〉〈title type="main"〉ResultsA significantly increased number of lymphocytes, mast cells and eosinophils was detected in the lamina propria in food-allergic patients and, in lower number, in atopic controls. Immunostaining for IL-5 was markedly positive in food-allergic patients, slightly increased in atopic controls and negative in nonatopic controls. Ultrastructurally, in food-allergic patients and in atopic controls, IL-5 was localized in eosinophil granules, in the matrix of intact granules and at the periphery of altered granules. Double immunofluorescent staining was performed in food-allergic patients and showed that 86.7% of IL-5+ cells were eosinophils, and that IL-5 was expressed by 24% of eosinophils. IL-5 mRNA was expressed in food-allergic patients but was not detected in atopic and nonatopic controls.〈section xml:id="abs1-4"〉〈title type="main"〉ConclusionActivated eosinophils are involved in gut atopic reactions occurring in food allergy and are probably in part upregulated by their own local production of IL-5.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Histopathology 42 (2003), S. 0 
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 132 (1995), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 14 (2000), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Crohn’s disease is associated with vascular injury and dysregulation of the intestinal immune system which together can provide disturbance of mesenteric circulation functional properties.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To evaluate the vascular reactivity of mesenteric arteries from patients with Crohn’s disease.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Phenylephrine-induced contractions were assessed from 10 patients with Crohn’s disease and 8 control organ donors. NG-nitro-L-arginine-methyl-ester (L-NAME) was used to test the presence of inducible NO synthase. Endothelium dependent and independent relaxation was assessed using acetylcholine, bradykinin, calcium ionophore A23187 and sodium nitroprusside.〈section xml:id="abs1-4"〉〈title type="main"〉Results:The contractile response to phenylephrine was significantly decreased in arteries without endothelium from patients with Crohn’s disease. Exposure to the NO synthase inhibitor L-NAME restored the contractile response to phenylephrine. Relaxation remained unaltered in both groups.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion:These data provide direct evidence for fading of contraction caused by phenylephrine in Crohn’s disease. The restored mesenteric artery tone by a specific NO synthase inhibitor suggests that an increased production for NO in vascular smooth muscle might be responsible of this altered vascular reactivity.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Keywords Type II diabetes ; peroxisome proliferator-activated receptor γ ; human pancreas ; islets ; beta cell ; thiazolidinediones ; troglitazone ; rosiglitazone.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Thiazolidinediones are reported to improve pancreatic islet morphology and beta-cell function in rodents, supporting the hypothesis of a direct action of thiazolidinediones on endocrine islet cells. In this study we examined the expression of the peroxisome proliferator-activated receptor γ, a nuclear receptor that is activated by naturally occurring fatty acids and synthetic thiazolidinediones, in normal human endocrine pancreatic cells. Methods. Human islets were isolated from pancreata harvested in ten brain-dead lean non-diabetic adult donors. We analysed the gene and protein expression of the human peroxisome proliferator-activated receptor γ and evaluated the effects of peroxisome proliferator-activated receptor γ agonist on insulin secretion in human islet preparations. Results. The RT-PCR carried out on total RNA from four distinct human islet preparations demonstrated the presence of peroxisome proliferator-activated receptor γ mRNA. Western blot analysis showed the consistent expression of peroxisome proliferator-activated receptor γ protein. Peroxisome proliferator-activated receptor γ was shown to be present in all three endocrine cell types studied (alpha, beta and delta cells) by immunohistochemistry. Conclusion/interpretation. We found that peroxisome proliferator-activated receptor γ is highly expressed in human islet endocrine cells, both at the mRNA and protein levels. These results support the hypothesis of a direct influence of peroxisome proliferator-activated receptor γ agonist on human pancreatic endocrine cells. [Diabetologia (2000) 43: 1165–1169]
    Type of Medium: Electronic Resource
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