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PubMed2004

[Polymorphonuclear leukocytes decrease the immunostimulatry capacity of human dendritic cells].

The aim of this work was to evaluate the ability of polymorphonuclear leukocytes (PMNL) to modulate the function of dendritic cells (DCs). Human DCs were used to analyze the effect of PMNL on DCs. The allostimulatory proliferation of T cells induced by DCs incubated with PMNL was lower (42 +/- 14%, n:8, p<0.05) compared with untreated DCs. The decreased proliferation correlated with lower IFNgamma production (DCs: 781 +/- 3 pg/ ml; DCs-CS: 343 +/- 178 pg/ml, p<0.05). The same effect was observed in an antigen specific assay. However, the effect was not observed when PMNL where incubated with mature DCs. Indeed, the effect of PMNL was partially reverted with serine proteases inhibitors. Overall, these results suggest that PMNL modulates DCs activity by serine proteases.

Antigens, CD↗

PubMed2002

Regulation of cardiac bradykinin B1- and B2-receptor mRNA in experimental ischemic, diabetic, and pressure-overload-induced cardiomyopathy.

Although kinins have been associated with the regulation of cardiovascular function in left ventricular hypertrophy (LVH) as a consequence of hypertension, myocardial infarction (MI), and/or diabetic cardiomyopathy, less is known about their receptor regulation under these conditions. We have therefore investigated the bradykinin B1-receptor (B1R) and B2-receptor (B2R) mRNA expression in rat models of MI, LVH and diabetes mellitus (DM). Sprague-Dawley rats (SD) were submitted to permanent ligation of the left descending coronary artery (LAD) to induce a MI, whereas DM was induced by a single injection of streptozotocin (STZ). LVH was induced after thoracic aortic banding (AB). Three weeks after MI, six weeks after STZ injection or six weeks after AB, left ventricular (LV) function was characterized using a Millar-tip catheter. Cardiac B1R- and B2R-mRNA expression were analyzed by specific RNase-protection assays (RPA). LV contractility (dP/dt max) was impaired by 40-48% in rats after induction of MI or DM compared to their controls. However, despite an enormous increase in LV end-diastolic pressure (LEVDP) to 310% after AB, LV contractility did not differ compared to the controls. These hemodynamic changes were accompanied by an up-regulation of cardiac B1R- (MI, 288%; STZ, 215%; AB, 4180%) and B2R-mRNA expression (MI, 122%; STZ, 288%; AB, 96%). Up-regulation of both BK-receptor (BKR) types in early stages of cardiac wound healing induced by ischemia and in chronic stages of cardiac remodeling induced by pressure-overload or by hyperglycemia indicates that kinins play a major role in the complex processes of cardiac tissue injury and repair.

Animals↗