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Background. Chronic obstructive pulmonary disease (COPD) is an airway inflammatory disease caused by inhalation of toxic particles, mainly cigarette smoking, and now is accepted as a disease associated with systemic characteristics. Objective. The aim of this work was to investigate and compare selected biochemical parameters in patients with and without COPD. Material and Methods. Observation group consisted of clinically stable patients with COPD (n = 60). The control group was healthy persons from the general population, without COPD, who were divided into two subgroups – smokers (n = 30) and non-smokers (n = 30). Laboratory parameters were investigated by automated clinical chemistry analyzer LISA 200th. Results. Albumin in our measurements showed an average value of 39.55 g.l-1 in the patient population; 38.89 g.l-1 in smokers and in non-smokers group 44.65 g.l-1. The average value of pre-albumin in the group of patients was 0.28 ± 0.28 g.l-1 and 0.30 ± 0.04 g.l-1 in smokers group. The average value of the orosomucoid in patients was about 1.11 ± 0.90 mg.ml-1. In the group of smokers, the mean value of orosomucoid was 0.60 ± 0.13 mg.ml-1. The level of C-reactive protein (CRP) in the patient group reached an average value of 15.31 ± 22.04 mg.l-1, in the group of smokers was 5.18 ± 4.58 mg. l-1. Prognostic inflammatory and nutritional index (PINI) in the group of patients showed a mean value of 4.65 ± 10.77 and 0.026 ± 0.025 in smokers. Conclusions. The results of this work show, that the values of index PINI in COPD patients are significantly higher than in smokers (P <0.001). This along with other monitored parameters indicative inflammation as well as a catabolic process that occurs in the organism of patients with COPD.
Recent studies indicate the involvement of peroxisone proliferator-activated receptor- (PPAR-) in the inflammatory reaction. The exact mechanism of PPAR- action has not been elucidated. It is supposed that PPAR- regulates transcription of genes responsible for encoding cytokines involved in the inflammatory response. The latest studies, carried out to explain the pathogenesis of non-specific colitis, confirm beneficial effects of PPAR- agonists on attenuation of colon inflammation. The aim of the present study was to assess the effects of nuclear PPAR- activity on the course of experimental acute colitis induced by intragastric administration of dextran sodium sulphate (DSS) using the PPAR- agonist rosiglitazone and the antagonist BADGE in rats. Colitis in Wistar rats was induced by 1.5% DSS administered in drinking water for 8 days. Animals with induced colitis received rosiglitazone, bisphenol A diglycidyl ether (BADGE) or both substances. After decapitation, colons were macroscopically and histopathologically evaluated. Levels of interleukin-1ß (IL-1ß), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor- (TNF-) and myeloperoxidase (MPO) were determined in serum and colon homogenates using ELISA. In rats with experimentally induced colitis receiving rosiglitazone, the inflammatory reaction was found to be markedly limited; ulceration, oedema and infiltration activity were reduced. The activated PPAR- inhibit the expression of proinflammatory factors, such as IL-6, TNF-, and neutrophil chemotaxis, which was evidenced by MPO reduction in serum and colon homogenates mediated by rosiglitazone. The positive effects of rosiglitazone on expression of IL-10 were also demonstrated. During the short period of observation, BADGE did not increase histopathological inflammatory markers.
The aim of this study was to evaluate the influence of pretreatment with the phosphodiesterase-4 inhibitor rolipram on pulmonary resistance, influx of inflammatory cells, and histamine concentration in bronchoalveolar lavage fluid (BALF) during an experimental asthmatic reaction induced in ovalbumin (OA)-sensitized guinea pigs, challenged with OA inhalation. The experiment was performed in three groups of guinea pigs: two experimental groups, pretreated with rolipram or dexamethasone, and a control group without any pretreatment. Lung resistance (LR) was continuously recorded under suppression of spontaneous breathing during early asthmatic reaction. BALF was obtained before and at three time points up to 24 hr after the challenge. In the untreated, control animals a transient, significant increase in neutrophils, total and CD4+ lymphocytes, macrophages, eosinophils, and in histamine concentration in BALF was noted. Pretreatment with rolipram significantly reduced LR, eosinophils infiltration, and histamine release into the bronchoalveolar space during the early asthmatic reaction. These effects were generally comparable with those of dexamethasone, except that dexamethasone also reduced the influx of neutrophils into BALF.
Rabbits exposed repeatedly to aerosols of endotoxin-containing microvesicles (ECMV) of the outer membrane of the Pantoea agglomerans strain isolated from airborne grain dust showed a large increase in the concentration of circulating cytokines: total interferon (IFN), interleukin-1 alpha (IL-1 alpha), and tumor necrosis factor alpha (TNF alpha). The increase was significantly higher compared to animals exposed to control saline (p<0.001). Aerosol exposure to ECMV also induced the formation of specific precipitin antibodies and lymphocyte activation. The results indicate strong immunomodulative properties of ECMVs produced in nature by Pantoea agglomerans bacteria, and heavily contaminating organic dusts.
The systemic inflammatory reaction (acute phase response) is induced by many nox­ious stimuli but in all cases the inflammatory cytokines, such as interleukin-1-beta (IL-1/ß) and interleukin-6 (IL-6), are involved. Liver cell response to inflammation manifested by a characteristic change in the profile of synthesized plasma proteins (acute phase proteins) has been extensively studied. Here we describe a model system of cultured human hepatoma HepG2 cells stimulated with IL-1/ ß to evaluate the trans­criptome induced by this cytokine during 24 h of treatment. By using differential dis­play analysis we found IL-1/ß-induced upregulation of several genes coding for cellular trafficking/motor proteins, proteins participating in the translation machinery or in­volved in posttranscription/posttranslation modifications, proteases, proteins in­volved in cellular metabolism, activity modulators, proteins of the cell cycle machin­ery and also some new proteins so far functionally not classified.
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