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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathophysiology of preeclampsia (PET) implicates an inflammatory dysfunction. This study profiled this host response by challenging whole blood with lipopolysaccharide. Multiplex immunoassays determined interleukin (IL)-1beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12(p70), IL-13, IL-17, granulocyte/granulocyte macrophage-colony stimulating factors (G-CSF/GM-SCF), interferon(IFN)-gamma, monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein-1beta and tumor necrosis factor (TNF)-alpha levels. Secretory capacity was expressed in pg/million white cells or monocytes (+/-SEM). PET featured significantly higher IL-1beta, IL-2, IL-10, IL-13, G-CSF, IFN-gamma, MCP-1 and TNF-alpha monocyte secretory capacities (p < 0.05). The PET group exhibited an inflammatory hyper-responsiveness (p < 0.01) which was poorly described by the traditional Th1:Th2 dichotomy.
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PMID:Host inflammatory response profiling in preeclampsia using an in vitro whole blood stimulation model. 1829

The mechanisms by which corticosteroids reduce airway inflammation are not completely understood. Traditionally, corticosteroids were thought to inhibit cytokines exclusively at the transcriptional level. Our recent evidence, obtained in airway smooth muscle (ASM), no longer supports this view. We have found that corticosteroids do not act at the transcriptional level to reduce TNF-alpha-induced IL-6 gene expression. Rather, corticosteroids inhibit TNF-alpha-induced IL-6 secretion by reducing the stability of the IL-6 mRNA transcript. TNF-alpha-induced IL-6 mRNA decays at a significantly faster rate in ASM cells pretreated with the corticosteroid dexamethasone (t(1/2) = 2.4 h), compared to vehicle (t(1/2) = 9.0 h; P < 0.05) (results are expressed as decay constants [k] [mean +/- SEM] and half-life [h]). Interestingly, the underlying mechanism of inhibition by corticosteroids is via the up-regulation of an endogenous mitogen-activated protein kinase (MAPK) inhibitor, MAPK phosphatase-1 (MKP-1). Corticosteroids rapidly up-regulate MKP-1 in a time-dependent manner (44.6 +/- 10.5-fold increase after 24 h treatment with dexamethasone; P < 0.05), and MKP-1 up-regulation was temporally related to the inhibition of TNF-alpha-induced p38 MAPK phosphorylation. Moreover, TNF-alpha acts via a p38 MAPK-dependent pathway to stabilize the IL-6 mRNA transcript (TNF-alpha, t(1/2) = 9.6 h; SB203580 + TNF-alpha, t(1/2) = 1.5 h), exogenous expression of MKP-1 significantly inhibits TNF-alpha-induced IL-6 secretion and MKP-1 siRNA reverses the inhibition of TNF-alpha-induced IL-6 secretion by dexamethasone. Taken together, these results suggest that corticosteroid-induced MKP-1 contributes to the repression of IL-6 secretion in ASM cells.
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PMID:Corticosteroids reduce IL-6 in ASM cells via up-regulation of MKP-1. 1831 42

Patients with bronchiectasis often have impaired quality of life (QoL), which deteriorates with exacerbations. The aim of this study was to investigate changes in QoL and how these were influenced by changes in airway physiology and inflammation in patients with bronchiectasis before and after resolution of an exacerbation. Sputum induction and a QoL questionnaire were undertaken on the first day, day 14, and 4 weeks after completion of intravenous antibiotics (day 42). Eighteen patients (12 female) were recruited, median (IQ range) age of 54 (47-60) years. There was a trend towards an improvement in lung function from visit 1 to visit 2, but this was not statistically significant. C-reactive protein (CRP) [mean (SEM)] reduced between visit 1 and visit 2 [55.4 (21.5) vs 9.4 (3.1) mg/L, P = 0.03] but did not increase significantly on visit 3 [44.4 (32.9) mg/L, P = 0.27]. The median (interquartile range) sputum cell count (x10(6) cells/g of sputum) decreased from visit 1 to visit 2 [21.6 (11.8-37.6)-13.3 (6.7-22.9) x 10(6) cells/g, respectively, P = 0.008] and increased from visit 2 to visit 3 [26.3 (14.1-33.6) x 10(6) cells/g, P = 0.03]. All soluble markers of inflammation significantly reduced from visit 1 to visit 2 but increased on visit 3 with the exception of TNF-alpha. Regarding QoL, three of the four domains (dyspnoea, emotional, mastery) significantly improved from visit 1 to visit 2 but did not change between visit 2 and visit 3. The improvements in QoL scores could not be explained by the improvements in lung function or inflammatory markers.
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PMID:Quality of life and inflammation in exacerbations of bronchiectasis. 1868 92

Leishmania has developed mechanisms to escape from immune defense of phagocytes by inhibiting microbicidal oxygen and nitrogen radicals. This work evaluated the influence of meglumine antimonate (Sb(V)) on the phagocyte functions involved in the defense against leishmania, through phagocytosis, reactive oxygen, nitrogen and TNF-alpha production in the absence or presence of the drug, in vitro. Meglumine antimonate increased the number of Saccharomyces cerevisiae ingested by monocyte and the percentage of these cells engaged in phagocytosis, which resulted in an increase of the monocyte phagocytic index by 158%. Meglumine antimonate also increased the number of S. cerevisiae ingested by neutrophil and the percentage of these cells engaged in phagocytosis, increasing the neutrophil phagocytic index by 219%. The median of percent reduction of NBT was significantly increased after treatment with this pentavalent antimony from 89.5% to 96.5%. Meglumine antimonate had no influence on nitric oxide production, but it significantly increased the mean+/-SEM production of tumor necrosis factor by 230%. However, monocytes incubated with TNF significantly increased NO production. This antimonial increased the phagocytic capacity of monocytes and neutrophils and enhanced superoxide anion production by phagocytes, which represent the first line of defense against the parasite. Furthermore, meglumine antimonate increased TNF, and via this cytokine, it may also indirectly increase NO production. Our data suggest that these immunomodulatory effects of meglumine antimonate may play a role in fighting leishmania and that meglumine antimonate provides the phagocytes with a mechanism that prevents leishmania from escaping immune defense.
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PMID:Meglumine antimonate directly increases phagocytosis, superoxide anion and TNF-alpha production, but only via TNF-alpha it indirectly increases nitric oxide production by phagocytes of healthy individuals, in vitro. 1869 97

The pathogenesis of chagasic cardiomyopathy is not completely understood, but it has been correlated with parasympathetic denervation (neurogenic theory) and inflammatory activity (immunogenic theory) that could affect heart muscarinic acetylcholine receptor (mAChR) expression. In order to further understand whether neurogenic and/or immunogenic alterations are related to changes in mAChR expression, we studied two models of Trypanosoma cruzi infection: 1) in 3-week-old male Sprague Dawley rats chronically infected with T. cruzi and 2) isolated primary cardiomyocytes co-cultured with T. cruzi and peripheral blood mononuclear cells (PBMC). Using [3H]-quinuclidinylbenzilate ([3H]-QNB) binding assays, we evaluated mAChR expression in homogenates from selected cardiac regions, PBMC, and cultured cardiomyocytes. We also determined in vitro protein expression and pro-inflammatory cytokine expression in serum and cell culture medium by ELISA. Our results showed that: 1) mAChR were significantly (P < 0.05) up-regulated in right ventricular myocardium (means +/- SEM; control: 58.69 +/- 5.54, N = 29; Chagas: 72.29 +/- 5.79 fmol/mg, N = 34) and PBMC (control: 12.88 +/- 2.45, N = 18; Chagas: 20.22 +/- 1.82 fmol/mg, N = 19), as well as in cardiomyocyte transmembranes cultured with either PBMC/T. cruzi co-cultures (control: 24.33 +/- 3.83; Chagas: 43.62 +/- 5.08 fmol/mg, N = 7 for both) or their conditioned medium (control: 37.84 +/- 3.84, N = 4; Chagas: 54.38 +/- 6.28 fmol/mg, N = 20); 2) [(3)H]-leucine uptake was increased in cardiomyocytes co-cultured with PBMC/T. cruzi-conditioned medium (Chagas: 21,030 +/- 2321; control 10,940 +/- 2385 dpm, N = 7 for both; P < 0.05); 3) plasma IL-6 was increased in chagasic rats, IL-1beta, was increased in both plasma of chagasic rats and in the culture medium, and TNF-alpha level was decreased in the culture medium. In conclusion, our results suggest that cytokines are involved in the up-regulation of mAChR in chronic Chagas disease.
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PMID:Trypanosoma cruzi infection induces up-regulation of cardiac muscarinic acetylcholine receptors in vivo and in vitro. 1882 Jul 70

Curdlan modified polyurethane was created by physically entrapping the former on TecoflexTM surface. ATR-FT-IR, SEM-EDAX and AFM analysis revealed the formation of stable thin curdlan layer on the film. Contact-angle measurements showed that the modified film was highly hydrophilic. Confocal laser scanning microscopy showed the existence of entrapped layer of approximately 20-25 microm in depth. Surface entrapment of curdlan minimized both protein adsorption and mouse L929 fibroblast cell adhesion relative to the control. Surface induced cellular inflammatory response was determined from the expression levels of proinflammatory cytokine TNF-alpha, by measuring their mRNA profiles in the cells using real time polymerase chain reaction (RT-PCR) normalized to the housekeeping gene GAPDH. The inflammatory response was suppressed on the modified substrate as expression of TNF-alpha mRNA was found to be up regulated on TecoflexTM, while it was significantly lower on curdlan substrate. The adhesion of S. aureus decreased by 62% on curdlan modified surface. Using such simple surface entrapment process, it will be possible to develop well-defined surface modifications that promote specific cell interactions and perhaps better performance in the long-term as implant.
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PMID:TecoflexTM functionalization by curdlan and its effect on protein adsorption and bacterial and tissue cell adhesion. 1909 93

Sulfobetaine-modified poly(ethylene terephthalate) (PET) systems were created by physically entrapping the zwitterionic species on the PET surface. The presence of the sulfobetiane molecules on these surfaces were verified by ATR-FTIR and SEM-EDAX analysis, while wettability of the films was investigated by water contact angle measurements. The blood compatibility of the modified films was evaluated by platelet adhesion in human platelet-rich plasma (PRP). The adhesion and inflammatory response of Mouse RAW 264.7 macrophage cells were studied. The surface induced cellular inflammatory response was determined by quantifying the expression levels of proinflammatory cytokines namely TNF-alpha and IL-1beta by measuring their mRNA profiles in the cells using real time polymerase chain reaction normalized to the housekeeping gene GAPDH. L-929 fibroblast cells were used to assess the propensity of the materials to support the fibroblast cell adhesion. A lower platelet adhesion and activation were observed on the sulfobetaine-modified PET film incubated in PRP after 2h when compared to control. The modified film reduced cellular adhesion events ( p<0.05) with respect to the base material, which could be linked to the reduced protein adsorption observed on this surface. The cellular inflammatory response was suppressed on sulfobetaine-modified substrate. Expression levels of pro-inflammmatory cytokines (TNF-alpha and IL-1beta) was found to be upregulated on bare PET, while it was significantly lower on modified PET ( p<0.001). Thus the sulfobetaine entrapment process can be applied on PET in order to achieve low biointeractions and reduced inflammatory host response for various biomedical and biotechnological applications.
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PMID:The biocompatibility of sulfobetaine engineered poly (ethylene terephthalate) by surface entrapment technique. 1974 1

One hundred and ninety-three Sprague-Dawley (SD) rats (average body weight 100-120g) were randomly divided into five groups (I-V). Groups I and II rats served as the negative and positive controls respectively and both received 0.1mg/kg Se from sodium selenite supplemented diets for the 18-week experimental period. Groups III-V rats were fed Se from SEM supplemented diets (0.3, 1 and 3mg/kg respectively). To induce hepatocarcinoma, groups II-V rats received diethylnitrosamine solution (100mg/L) at the dosage of 10mg/kg body weight in drinking water daily for 16 weeks, followed by sterilized water for a further 2 weeks. Group I rats received sterilized water throughout. At weeks 4, 8, 12 and 16 five rats in each group were sacrificed by cervical decapitation. At the termination of the study, at week 18, the surplus rats were sacrificed by cervical decapitation. Feed was withheld from the rats for 12 h before sampling. The following items including TNF-alpha, IGF-II, NO and T-NOS levels in plasma were tested using kit techniques. At the same time the expression of vascular endothelial growth factor (VEGF) in tumor tissue was analyzed by immunohistochemistry using the envision two-step methods with a kit. The results indicated that SEM could increase the levels of TNF-alpha in the early stages of hepatocarcinoma formation, however there was a decrease in the later stage of hepatocarcinogenesis. SEM could also significantly decrease the levels of IGF-II and NO, and inhibit the expression of VEGF in tumor tissue. SEM delayed the development of hepatocarcinoma in rats and that could be partially attributed to inhibition of angiogenesis.
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PMID:Effect of selenium-enriched malt on VEGF and several relevant angiogenic cytokines in diethylnitrosamine-induced hepatocarcinoma rats. 2012 81

The aim of the present study was to examine the effect of 1,25(OH)2D3 (calcitriol) on SMC (smooth muscle cell) migration, especially in the context to atherogenesis. SMCs were obtained from the aortas of newborn Wistar rats by enzymatic digestion. Different aspects of cell behavior during migration in culture were examined by phase contrast, fluorescence and electron microscopy (TEM, SEM) and supported by flow cytometric and biochemical analyses. Morphological studies revealed that supra-physiological (1-100 nmol/l) concentrations of calcitriol inhibit SMC differentiation, therefore these cells display several hallmarks of the synthetic state. Dynamic changes in actin cytoskeleton organization were a critical event in SMC shape, adhesion and spreading. Calcitriol diminished stress fibers assembly and focal adhesions formation. Reduced expression of beta1-integrin receptors on SMC surface after exposition to calcitriol coincided with increased proliferative and migratory activities of these cells. Moreover, after calcitriol stimulation, the ability of SMCs to the production of proinflamatory cytokines IFN-gamma, TNF-alpha and IL-6 was inhibited. The results from these comparative investigations indicate that 1,25(OH)2D3 inhibit differentiation and facilitate SMC migration in culture. It has been also suggested that such responses of SMCs to calcitriol play a beneficial role in fibrous cap formation during atherosclerotic process.
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PMID:Increased migratory properties of aortal smooth muscle cells exposed to calcitriol in culture. 2030 64


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