ABSTRACT
Objectives: Preeclampsia [PE] is associated with impaired decidual leukocyte and plasma cytokine balance compared with normal pregnancy. We aimed to investigate maternal plasma levels of Interferon-gamma [IFN-g], Tumor Necrosis Factor-alpha [TNF-a], Transforming Growth Factor-beta [TGF-b], Interleukin-4 [IL4], IL6, IL10, IL17, IL35, suppressor of Cytokine Signalling-3 [SOCS3] and placental bed leukocytes in preeclamptic and healthy pregnants
Materials and Methods: This study was conducted with 40 preeclamptic and 40 normotensive pregnants. Cytokine levels were studied with enzyme-linked immunosorbent assay. CD8, CD56 and CD163 antigens were analysed by immunohistochemical study on placental bed biopsies
Results: In preeclamptic women; IFN-g and TGF-b levels were significantly higher and IL-35 levels were significantly lower than those of controls. CD8, CD56 and CD163 positivity of preeclamptic group were not significantly higher than those of controls. CD8 staining showed negative correlation with plasma IL17 levels. CD163 staining showed negative correlation with TNF-a/IL4 ratio. TNF-a/IL4 ratio showed minimal influence on placental bed CD163 staining
Conclusion: Slightly increased placental bed CD8, CD56 and CD163 positive leukocytes and increased plasma IFN-g, TGF-b and decreased plasma IL35 levels of preeclamptic pregnants indicate an aberrant cell mediated immunity in PE. We could not say yet that this condition is whether result or reason. New studies are needed to discuss our results
ABSTRACT
Endothelin (ET) receptor antagonists have been developed to produce a reduction of ET related effects in various diseases, as well as in animal models of airway inflammation. We aimed to investigate the anti-inflammatory potential of bosentan on a rat model of emphysema. Thirty Wistar male rats were classified as control group (group 1), intratracheally (i.t.) instilled with saline, treated with vehicle solution; elastase group (group 2), i.t. instilled with porcine pancreatic elastase (PPE), treated with vehicle solution; and PPE+bosentan group (group 3), i.t. instilled with PPE, treated with bosentan. The levels of TNF-alpha, IL-1beta, IL-6, and IL-8 in bronchoalveolar lavage fluid (BALF) and lung tissue, cell counts in BALF, and histologic analysis of all groups were evaluated. Neutrophile granulocytes (NG) and alveolar macrophages (AM) were increased more in group 2 than in group 1 (P<0.001, P=0.04, respectively). Compared with group 2, neutrophil granulocyte (NG) and alveolar macrophages (AM) counts were decreased in group 3 (P< 0.001). Histological examination confirmed a diffuse neutrophilic inflammation and irregular alveolar air space enlargement in group 2. Treatment with bosentan partially reduced the enlarged lung volumes. Compared with group 1, the BALF levels of TNF-alpha and IL-6, and the lung tissue levels of IL-1beta, IL-6, and IL-8 were increased in group 2 (P=0.028, P=0.005, P=0.001, P=0.019, P<0.001, respectively). The TNF-alpha and IL-8 levels of BALF (P=0.007, P=0.001, respectively), and the TNF-alpha, IL-1beta, IL-6, and the IL-8 levels of lung tissue (P=0.031, P=0.017, P=0.007, P<0.001) were decreased in group 3 compared to group 2. In conclusion, bosentan decreased the inflammatory response by reducing numbers of inflammatory cells and proinflammatory cytokines.