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Kinins, universal mediators of inflammation, are recognized by two kinds of receptors, B1 and B2, which have been found to be expressed in numerous cell types of several species. However, the knowledge of the regulation of these receptors in leukocytes is still not satisfactory. In the current work, we have demonstrated a constitutive production of B2 receptor mRNA in the human promonocyte U937 cells and its two-fold augmentation after cell differentiation with retinoic acid and phorbol ester. Bradykinin and des-Arg10-kallidin induced the expression of both B2 and B1 receptors in cells before and after differentiation. Generally, the undifferentiated cells were more susceptible to bradykinin-dependent induction of kinin receptors (increases by approximately 250% and 200% for B2 and B1 receptors, respectively). The induction, by approx. 200%, of B1 receptor by des-Arg10-kallidin was detected on both mRNA and protein levels. In addition, an unexpected strong induction of B2 receptor by this compound was observed in the retinoic acid- and phorbol ester-differentiated cells (by 150% and 200%, respectively) that suggests a possible autoregulation of kinin receptors by own agonists during the inflammatory state. On the other hand, a strong enhancement of the expression of both receptors by interleukin 1β, especially in the phorbol ester-differentiated cells, indicates the involvement of kinin receptors in the propagation of the inflammatory processes.
The effects of lysozyme dimer (2 and 20 μg/kg) administered i.p. once and four times to mice on the phagocytic and killing ability of peritoneal macrophages, interleukin-1 (IL-1) production by murine macrophages stimulated in vitro with lipopolisaccharide of E. coli and expression of thymocyte, splenocyte and mesenteric lymphonode cell CD3+, CD4+ and CD8+ markers were studied. It was found that lysozyme dimer administered once or four times at doses of 2 (μg/kg and 20 μg/kg augments the phagocytic and killing activity of peritoneal macrophages. The strongest stimulating effect was noted after four injections of lysozyme dimer at a dose of 20 μg/kg. Moreover, lysozyme dimer is able to modulate the production of IL-1 by murine macrophages stimulated in vitro with LPS. Exposure to four doses of lysozyme dimer (20 μg/kg) enhances the synthesis and release of IL-1, but this drug administered once (2 μg/kg and 20 μg/kg) or four times (2 μg/kg) decreases IL-1 production by peritoneal macrophages. It was also found that administration of lysozyme dimer at a dose of 20 μg/kg, irrespective of the number of doses applied, increases the percentage of CD4+ thymocytes and splenocytes. Moreover, exposure to four doses of lysozyme dimer (2 and 20 μg/kg) increases the percentage of CD4+ and CD8+ mesenteric lymphonode cells.
Content available remote Glial scar instability after brain injury
Glial scar is formed following surgical damage to the cerebral cortex. In the present study we examined the ultrastructural status of the cerebral cortex 14 to 180 days following surgical damage to cerebral parenchyma. The results showed a contribution of astrocytes, but also mesodermal cells, to the process of scar formation. Furthermore, our study showed that the process initiated by trauma did not terminate with the formation of a glial scar. Late phases of repair following tissue damage were associated with lytic processes and a disassembly of the cerebral parenchyma. These findings indicate a changing and unstable nature of the glial scar and its components.
The interaction of adrenergic agonists and/or antagonists with the adrenergic receptors expressed on immunologically active cells including macrophages plays an important role in regulation of inflammatory responses. Our study investigated the effects of carvedilol, a unique vasodilating b-adrenergic antagonist, and endogenous adrenergic agonists (adrenalin, noradrenalin, and dopamine) and/or antagonists (prazosin, atenolol) on lipopolysaccharide-stimulated nitric oxide (NO) production from murine macrophage cell line RAW 264.7. The production of NO was determined as the concentration of nitrites in cell supernatants (Griess reaction) and inducible nitric oxide synthase (iNOS) protein expression (Western blot analysis). Scavenging properties against NO were measured electrochemically. Carvedilol in a concentration range of 1, 5, 10 and 25 µM inhibited iNOS protein expression and decreased the nitrite concentration in cell supernatants. Adrenalin, noradrenalin or dopamine also inhibited the iNOS protein expression and the nitrite accumulation. Prazosine and atenolol prevented the effect of both carvedilol and adrenergic agonists on nitrite accumulation and iNOS expression in lipopolysaccharide-stimulated cells. These results, together with the absence of scavenging properties of carvedilol against NO, imply that both carvedilol and adrenergic agonists suppress the lipopolysaccharide-evoked NO production by macrophages through the activation and modulation of signaling pathways connected with adrenergic receptors.
Since C. pseudotuberculosis is a facultative intracellular pathogen the aim of this study was focused on evaluating mechanisms that allowed these bacteria to survive in macrophages and determining their influence on induction of cell death. The influence of Corynebacteria on the programmed cell death of macrophages was determined on the basis of induction the autophagy and apoptosis in the cultures of murine macrophage cell lines J774 infected with bacteria. Corynebacterium pseudotuberculosis strains could survive within macrophages more than 48 hours. During that time bacteria were released as a result of the process that lead to death of phagocytes. This property varied among studied strains. There was no increase of micro- tubule-associated protein I light chain 3 (MAP I LC3) activity in macrophages infected with examined strains comparing with uninfected cultures and cultures treated with autophagy inducer (rapamycin) that served as negative and positive controls, respectively. The study with confocal microscopy did not show the increasing of caspase-3 activity in the infected macrophages and their nucleus did not reveal the fragmentation.
Badano proces degradacji kwasu poli(L-mlekowego) w obecności makrofagów (Mf) oraz biozgodność układu PLLA+Mf. Postęp degradacji oceniano na podstawie pomiarów lepkości polimeru, analizy widm w zakresie podczerwieni oraz oznaczenia ilości uwalnianego kwasu mlekowego. Porównano żywotność makrofagów oraz sekrecję cytokin w hodowlach makrofagów w nieobecności biomateriału oraz w układach zawierających filmy PLLA i makrofagi. Stwierdzono wzrost szybkości degradacji PLLA w obecności makrofagów oraz zadowalającą biozgodność poli(kwasu L-mlekowego) i komórek linii makrofagowej.
The process of degradation of poly(L-lactic acid) (PLLA) in the presence of macrophages (Mf) and the biocompatibility of the system PLLA+Mf was studies. The progress of the degradation was monitored by the measurements of polymer viscosity and IR spectra of the films as well as the concentration of the released lactic acid. The viability of macrophages and the secretion of cytokines were compared for the systems containing PLLA films immersed in macrophage suspension and macrophages cultured without the polymer. The results confirm the increase in the rate of PLLA degradation in the presence of macrophages as well as the satisfactory biocompatibility of poly(L-lactic acid) and macrophage cells.
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