Deregulation of cyclo-oxygenase isozyme expression has been shown to be a consistent feature of inflammatory bowel diseases and colorectal cancer in humans. This study investigated the cellular localization of aberrant cyclo-oxygenase expression in normal and diseased colon. Biopsies of seven normal colonic tissues, eight tissue samples from patients suffering from Crohn's disease, five polyps from patients with familiar adenomatous polyposis coli, and ten sporadic adenocarcinomas were analyzed using isozyme-selective immunoprecipitation, western blotting, and immunohistochemistry. Cyclo-oxygenase-1 expression was demonstrated in normal human colon, Crohn's disease, and colorectal tumors. In normal colon and also in adenomatous polyps, cyclo-oxygenase-1 specific immunosignals were localized to epithelial cells of the upper part of the crypts and endocrine cells of the lower part. In Crohn's disease cyclo-oxygenase-1 expression was restricted to cells of the inflammatory infiltrate. While barely detectable in normal colon, cyclo-oxygenase-2 protein was strongly increased in epithelial cells located in the uppermost part of the crypts, in surface epithelial cells, and in mononuclear cells of the lamina propria of Crohn's disease. The constitutive overexpression of cyclo-oxygenase-2 protein observed in the majority of the adenomatous polyps and all adenocarcinomas was attributed to both epithelial and interstitial cells in that the latter predominated in adenomas, and epithelial cells were the prevailing cyclo-oxygenase-2 expressing cell type in adenocarcinomas. In conclusion, both autocrine and paracrine effects of aberrant cyclooxygenase-2 expression may contribute to the development of Crohn's disease and colonic tumor development.
BackgroundTh2-type T cell response has a considerable role in atopic diseases. The involvement of Th17 and IL-17 in atopy process provided new understanding of allergic diseases. Bronchial hyperresponsiveness is quite common in allergic rhinitis. We aimed to explore the expression of IL-17 producing CD3+ CD4+ T cells in peripheral blood of rhinitic patients, with/without bronchial hyperresponsiveness and sensitized to common allergens, as this relationship has not been examined.MethodsSixty one patients with allergic rhinitis and thirty controls were examined. IL-17 producing T cells were detected by flow cytometry, IL-17, IL-4 and IL-13 levels in peripheral blood were evaluated by ELISA. Bronchial hyperresponsiveness was investigated with methacholine challenge test. Atopy was evaluated by skin prick tests with common allergens.ResultsIL-17 producing T cell percentage of AR group was significantly higher: 2.59 ± 1.32 than in controls 1.24 ± 0.22, (p = 0.001). Significant sex related difference in CD3+ CD4+ IL-17 T cells was observed: respectively in male patients versus female 3.15 ± 1.8% and 2.31 ± 0.9%, (p = 0.02). Rhinitics had greater bronchodilator responses compared to controls (p = 0.001), however the percentages of T cells in both groups appeared equal. Serum IL-17 levels in AR group were significantly higher (5.10 ± 4.40) pg/ml than in controls (3.46 ±1.28) pg/ml, (p = 0.04). IL-4 levels (0.88 ± 1.27) and IL-13 levels (3.14 ± 5.85) in patients were significantly higher than in control’s (0.54 ± 0.10) pg/ml, (p = 0.001) and (1.19 ± 0.64) pg/ml; (p = 0.001) respectively.The percentages of T cells in patients sensitized to 5 allergens (group I) were significantly lower (1.91 ± 0.62) than those sensitized to more than 5 allergens (group II) (2.91 ± 1.5) (p = 0.004).ConclusionsThe observed higher levels of IL-17 producing T cells in polysensitized males suggest a role of IL-17 in pathogenesis of AR. The higher airway responsiveness in AR may not be Th17 dependent. The higher serum values of IL-17, IL-4 and IL-13 demonstrate the presence of cytokine balance in atopic diseases.
Our aim was to investigate the CD40-CD40 ligand system in preeclamptic women. We also studied CD62P and platelet-monocyte aggregates, which have been closely linked to the CD40-CD40L system. Platelet expression of CD40L and CD62P and expression of CD40 on monocytes and platelet-monocyte aggregates were determined by flow cytometry in whole blood from 23 preeclamptic women, 23 normotensive pregnant women, and 23 nonpregnant women. The preeclamptic women showed a significant increase in CD40L and CD62P on platelets and in CD40 on monocytes when compared with normotensive pregnant women and nonpregnant women (all P < .001). There was a significant increase in platelet-monocyte aggregates in preeclamptic women (P < .001) and normotensive pregnant women (P = .003) compared with nonpregnant women. Preeclampsia is associated with activation of the CD40-CD40L system. The activation of this system may contribute to the development or maintenance of the proinflammatory and prothrombotic milieu found in preeclampsia.
The aim of our study was to investigate the significance of platelet-leukocyte aggregates (PLA) in women with recurrent pregnancy loss (RPL) as well as to identify association between common thrombophilic factors and whole blood levels of PLA in these patients. We measured PLA by whole blood flow cytometry in 66 nonpregnant women with hereditary and/or acquired thrombophilia and RPL, classified to 3 study groups, according to the type of losses (first, second, and third trimester) and 35 age-matched healthy controls. Platelet-leukocyte aggregates levels in all study groups were significantly increased compared to the control group (median values 2.13%, 2.32%, and 2.41%, vs median value in the control group 1.39%, P < .05 for all comparisons). Women with a single thrombophilic factor and women with combination of thrombophilic factors did not differ significantly as regards the PLA levels (2.13% vs 2.27%, P = .4). This study suggests that PLA may have a role in the pathogenesis of RPL in women affected by hereditary or acquired thrombophilia.
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