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Background: Cardiac surgical operation is followed by the development of inflammatory reaction. This reaction is regulated in many ways including the production of antiinflammatory cytokines such as IL-10 to avoid potentially harmful effects of inflammation., Methods and Results: We compared serum levels of cytokines IL-10, IL-6, and IL-13 in the group of patients undergoing cardiac surgical operation using either cardiopulmonary bypass (CPB, n=17) or surged on the beating heart (n=17). We found significant elevation in the serum level of IL-10 during surgery with the peak immediately after finishing surgery in CPB patients and at the first postoperative day in non-CPB patients, respectively. There is statistically significantly higher level of IL-10 in CPB patients in comparison with non-CPB patients at the end of surgery. Serum level of IL-6 is elevated in both groups during surgery reaching maximum immediately after surgery in CPB patients and at the first postoperative day in patients without CPB, respectively. The serum levels of IL-13 are only nonsignificantly changed during operation and in postoperative period in both groups., Conclusions: The intensity of inflammatory response in CPB patients which is enhanced by massive contact activation of blood and extensive ischemia-reperfusion injury is regulated by the production of antiiflammatory IL- 10 cytokine.

The zinc finger transcription factor Egr-l plays an important role in cardiovascular biology. While binding complementary motifs on DNA in the target genes, Egr-1 either increases or decreases proteosynthesis of many proinflammatory and antiinflammatory mediators. In physiologic circumstances, these mediators support healing and regeneration of damaged tissue, mainly by conducting angioneogenesis. In pathologic circumstances these same mediators take an active part in promoting tissue injury. The participation of the transcription factor Egr-1 in the pathogenesis of atherosclerosis can be traced from the initial phases with the generation of foam cells as far as the onset of acute cardiovascular or cerebrovascular ischemic events. At the same time, transcription factor Egr-1 presents a would-be linker at the level of which converge many seemingly heterogenous atherogenic risk factors such as hyperlipidemic disorders, untoward rheologic changes of blood flow often encountered in arterial hypertension or various infectious agents, with Chlamydia pneumoniae belonging to the most deeply investigated ones. Protective effects of the known anti-atherogenic factors, such as the endogenous antiinflammatory cytokine interleukin-10 or the "pleiotropic" effects of statins can be, at least in part, explained by their inhibitory influence on the activities of the transcription factor Egr-1.

Vascular endothelium, monocytes and T-lymphocytes belong to the key cellular populations, which take an active part in the host's defence reactions. A successful course of these reactions is determined by a meticulous control of all phases since the very first steps until final healing of all incurred wounds. Any failure of the control mechanisms may lead to the development of chronic inflammatory diseases with an autoimmune component, such as the rheumatoid arthritis or atherosclerosis. An inflammatory reaction which is already under way is regulated by anti-inflammatory cytokines. However, of equal importance is the maintenance of cellular participants of inflammatory reactions in a quiescent state while no pro-inflammatory stimuli are present. One of the most important endogenous mediators, which prevent a self-initiated activation of endothelial cells, monocytes and T-lymphocytes, is represented by the transcription factor Krüppel-like factor 2. Its impact on the mentioned cells is almost identical with the so-called pleiotropic effects of inhibitors of the enzyme HMG CoA reductase or statins. This review article offers an insight into basic preventive mechanisms exerted by KLF2, notably those related to atherosclerosis.

The most important set of receptors for danger patterns are TLR receptors. Together ten different TLR receptors were identified so far. Majority of TLR receptors is expressed on the cell surface to identify extracellulary localized danger signals. Some TLR receptors are also expressed in the intracellular compartment to identify intracellular danger signals. Receptors for danger signals display individual differences delineated by genetic polymorphism. The individual immune reactivity is developed in the context of genetic predisposition and the exposition to variable environmental factors. The differences in an individual immune reactivity are probably responsible for individual susceptibility or resistance to the development of immunopathological reactivity, which is involved in the immunopathogenesis of atherosclerosis.

Cellular and humoral components of innate immunity are able to identify danger signals both of the exogenous and endogenous origin. Exogenous danger signals are evolutionary conserved mosaics of danger patterns which are frequent in pathogenic microbes. Endogenous danger signals are raised during damage of self structures, by oxidative stress and/or by chemical modification of self molecules. Danger signals are identified by several families of molecules which are expressed on the surfaces of innate immunity cells. Among them the TLR receptors family which is associated with intracellular signaling pathway NF-kappaB is one of the most important. The inflammatory response is induced via activated NF-kappaB transcription factor.

Background: P-gp, MRP, LRP, Bcl-2, and Bax proteins play an important role in the multidrug resistance of leukemic cells. P-gp, MRP, and LRP proteins decrease the intracellular drug concentration, Bcl-2 and Bax proteins influence the apoptosis process. The overexpression of some of these proteins is associated with poor prognosis of leukemia. The aim of this study was to find the relationship between some multidrug resistance markers and some clinical and laboratory parameters. We compare also P-gp expression between acute myeloid leukemia (AML) FAB subgroups M0-M6., Methods and Results: With use of flow cytometry we measured the expression of P-gp, MRP, LRP, Bcl-2, and Bax proteins in acute myeloid leukemia patients cells. The study proved the association between blast percentage and P-gp protein expression (p=0.015) and the association between blast percentage and Bcl-2 protein expression (p=0.041). It was also shown the tendency of the LRP protein expression to associate with higher age of patients (p=0.062). Another correlation between MRP and Bax expression (p=0.006), as well as between LRP and Bax expression was found (p=0.034). In AML M0 FAB subgroup of patients the trend to higher P-gp protein expression was observed., Conclusions: The laboratory methodology to multidrug resistance markers detection was introduced. Some relations between multidrug resistance markers playing role in acute myeloid leukemia patients prognosis were suggested.

Resistance to cytotoxic drugs is a serious drawback in the treatment of patient with tumours, both of the haemopoietic and non-haemopoietic origin. The cytotoxic effect of drugs on the malignant cells manifests as the process of apoptosis. In the resistant malignant cells, apoptosis becomes prevented by several mechanisms. The multidrug resistance (MDR) is one of the principal mechanisms when the cancer cells develop resistance to multiple chemically and functionally unrelated cytotoxic compounds. The decrease of the cytotoxic drug concentration at the molecular target site may come from activation of some efflux membrane systems participating in the transport of cytotoxic drugs out of the cell (e.g. Pgp, MDR, and LRP). Another mechanism of resistance is the increased enzymatic detoxification of the drug by glutathion-S-transferase system. Changes in the molecular target of the cytotoxic drug such as topoisomerase molecule can be also responsible for the resistance. At least two additional mechanisms of resistance of tumour cells were identified. Resistance can come from either deregulation of proapoptotic mechanisms in tumour cells or by increased activity of reparation processes which control the damaged molecule of DNA. Several methods that detect the cause of resistance in distinct cell populations have been developed. The great effort is now focused on both the detection of mechanisms of the resistance and on the clinical procedures of overcoming the resistance to cytotoxic drugs.

Resistance to cytotoxic drugs is a serious drawback in the treatment of patients with tumours, both of the haemopoietic and non-haemopoietic origin. The cytotoxic effect of drugs on the malignant cells manifests as the process of apoptosis. In the resistant malignant cells, apoptosis becomes prevented by several mechanisms. The multidrug resistance (MDR) is one of the principal mechanisms when the cancer cells develop resistance to multiple chemically and functionally unrelated cytotoxic compounds. The decrease of the cytotoxic drug concentration at the molecular target site may come from activation of some efflux membrane systems participating in the transport of cytotoxic drugs out of the cell (e.g. Pgp, MDR, and LRP). Another mechanism of resistance is the increased enzymatic detoxification of the drug by glutathion-s-transferase system. Changes in the molecular target of the cytotoxic drug such as topoisomerase molecule can be also responsible for the resistance. At least two additional mechanisms of resistance of tumour cells were identified. Resistance can come from either deregulation of proapoptotic mechanisms in tumour cells or by increased activity of reparation processes which control the damaged molecule of DNA. Several methods that detect the cause of resistance in distinct cell populations have been developed. The great effort is now focused on both the detection of mechanisms of the resistance and on the clinical procedures of overcoming the resistance to cytotoxic drugs.

Resistance to cytotoxic drugs is a serious drawback in the treatment of patients with tumours, both of the haemopoietic and non-haemopoietic origin. The cytotoxic effect of drugs on the malignant cells manifests as the process of apoptosis. In the resistant malignant cells, apoptosis becomes prevented by several mechanisms. The multidrug resistance (MDR) is one of the principal mechanisms when the cancer cells develop resistance to multiple chemically and functionally unrelated cytotoxic compounds. The decrease of the cytotoxic drug concentration at the molecular target site may come from activation of some efflux membrane systems participating in the transport of cytotoxic drugs out of the cell (e.g. Pgp, MDR, and LRP). Another mechanism of resistance is the increased enzymatic detoxification of the drug by glutathion-S-transferase system. Changes in the molecular target of the cytotoxic drug such as topoisomerase molecule can be also responsible for the resistance. At least two additional mechanisms of resistance of tumour cells were identified. Resistance can come from either deregulation of proapoptic mechanisms in tumour cells or by increased activity of reparation processes which control the damaged molecule of DNA. Several methods that detect the cause of resistance in distinct cell populations have been developed. The great effort is now focused on both the detection of mechanisms of the resistance and on the clinical procedures of overcoming the resistance to cytotoxic drugs.

The diversity and heterogeneity of biologic reactions is a condition sine qua non for the adaptation of live organisms to changes of external environment. Reactions of the immune system enable survival even in extreme conditions. Modern medicine often reaches situations never met by the organism in phylogenesis. Thanks to up-to-date therapeutical approaches many patients survive with grave symptoms such as multiple organ failure and extensive forms of injury. New infectious diseases are emerging, e.g. HIV/AIDS. Notwithstanding the broad array of external insults, it becomes obvious that organisms mobilize defence reactions according to a general scheme. Likewise, exhaustion of the immune potential occurs according to an archetypal pattern. In the case of cell-mediated immunity the faultless course of which is of critical importance for organisms in extreme conditions, the loss begins with the absence of reactivity of T-cells to specific antigens to end with the absence of their reactivity to polyclonal mitogens. The article deals with pathogenic mechanisms underlying the onset of immunodeficiencies caused by both infectious and non-infectious stimuli with special regard being focused on cardiac surgery in extracorporeal circuit.

Background: Detection of membrane molecules by immunophenotypisation is a routine counterpart of the laboratory tests which are needed for the complex diagnostic procedures of hematopoetic malignancies at present. The immunochemical detection of intracellular molecules is essential in such cases, where the expression of surface molecules on malignant cells is poor, or where the results of other diagnostic analyses are unequivocal (cases with ectopic expression of other lineage-specific molecules and cases of biphenotypic leukemias)., Methods and Results: We followed the procedure using 4% solution of paraformaldehyd in phosphate buffered saline for fixation of cells. Lysing solution G (Becton-Dickinson) was used for permeabilisation of cells to detect nuclear and cytoplasmatic molecules. The permeabilised cell suspension was than washed with 0.5% solution of Tween 20 in phosphate buffered saline. This simple and rapid procedure is readily available for the routine detection of intracellular molecules. This approach is important for the diagnosis of hematopoetic malignancies.

Background: CagA antigen of Helicobacter pylori is highly immunogenic in humans. There is an increasing evidence that infection with CagA-positive strains is related to the development of peptic ulcer disease, atrophic gastritis, or gastric cancer. The aim of our study was to assess seropositivity to CagA in a group of 95 clinically symptomatic adults who underwent gastroduodenoscopy and to correlate results to their disease characteristics., Methods and Results: Serum immunoglobulin G antibodies to CagA detected by ELISA kit (Helicobacter p120, Viva Diagnostika, Germany) were compared to standard IgG specific antibodies against a pool of H. pylori antigens Synelisa Pin plate, ELIAS, Germany). Immunoglobulin G antibodies to CagA were present in 5/31 (16%) serum samples from H. pylori negative persons and 10/28 (36%) serum samples from H. pylori positive patients without peptic ulcer disease compared with 8/11 (73%) H. pylori positive patients with peptic ulcer disease in the past, 11/13 (85%) H. pylori positive patients with duodenal ulcers or duodenitis and 4/5 (80%) H. pylori positive (1/7, 14% H. pylori negative) serum samples from patients with gastric resection for peptic ulcers in the past. Serum levels of antibodies to CagA in the groups of patients with peptic ulcer disease in the past, with present duodenal ulcers of duodenitis and in H. pylori infected patients with gastric resection were significantly higher then those of H. pylori infected patients without peptic ulcer disease (P < 0.05). On the other hand, there was no significant difference in the presence of the specific antibodies against at pool of H. pylori antigens between these four groups., Conclusions: These data suggest that serologic response to the CagA antigen is more prevalent in H. pylori positive persons with present or past peptic ulceration than among infected persons without peptic ulcer disease. The presence of antibodies to CagA in H. pylori positive persons may be useful for the identification of patients with higher risk or more severe disease.

Homeostasis is mediated through interactions of adhesion molecules on the surface of platelets which belong into the families of selectins, integrins and immunoglobulins with soluble plasma proteins, surface molecules of activated endothelial cells and molecules of extracellular matrix. The membrane expression of some adhesion molecules (P-selectin) which are the part of granular system of resting platelet identify activated platelet. Adhesion molecules of platelets could be detected by immunochemistry through flow cytometry. By this approach the inherited defects of adhesion molecules on platelets and the activated platelet could be detected. The detection of activated platelets is very useful in many clinical conditions.

Background: Sjögren's syndrome (SS) is considered an autoimmune immunopathological disease, which is characterized by disorders of humoral and cell-mediated immunity. The objective of the work was to assess the ratio of T and B lymphocytes, subpopulations of T lymphocytes and NK cells in the peripheral blood of patients suffering from SS., Methods and Results: The investigated group was formed by 22 patients with the diagnosis of primary SS (mean age 55.7 years, range 39-83 years), 17 patients with the diagnosis of secondary SS (mean age 60.5 years, range 45-79 years). The ration of CD3-, CD4-, CD8-, CD19-, CD5-, CD25- HLA DR- cells in full blood was assessed by the monoclonal antibody technique of direct immunofluorescence, using evaluation by means of a flow cytometer. The results were compared by statistical methods with a control group of blood donors using Student's t-test, A relative increase of the ratio of CD3- T lymphocytes was revealed in patients with primary SS (75.3 +/- 17.9 %, p = 0.380) and secondary SS (73.7 +/- 11.8, p = 0.326), as compared with controls (65.3 +/- 10.3%). The absolute number of the subpopulation of suppressor helper inducer CD4+ T lymphocytes was markedly lower in patients with primary SS (0.056 +/- 0.27 - 10(9)/l, p = 0.0154), as compared with controls (0.81 +/- 0.27, 10(9)/l. The relative number of suppressor cytotoxic CD8- T lymphocytes was significantly higher in patients with primary SS (33.7 +/- 15.0%, p = 0.0001 and secondary SS (30.5 +/- 11.0%, p = 0.0002), as compared with controls (17.2 +/- 6.0%). The absolute number of inhibitory cytotoxic T lymphocytes was significantly higher in patients with primary SS (0.47 +/- 0.3. 10(9)/1, p = 0.0084) and patients with secondary SS (0.48 +/- 0.3, 10(9)/l, p = 0.0072). The relative number of CD57+ NK cells was significantly higher in patients with primary SS (21.1 +/- 11.0%, p = 0.0001) and secondary SS (19.3 +/- 11.7%, p = 0.0023). The absolute number of NK cells was significantly higher in patients with primary SS (0.28 +/- 0.20, 10(9)/l, p = 0.0025 and in patients with secondary SS (0.31 +/- 0.23, 10(9)/l, p = 0.01)., Conclusions: The revealed statistically significant increases in the number of T lymphocytes in patients with Sjögren's syndrome is probably caused by a significant increase of the subpopulation of CD8+ suppressor cytotoxic T lymphocytes. The latter probably overlap with the population of NK cells. These immunological abnormalities are even more marked in patients with primary Sjögren's syndrome due to the decrease of the absolute number of CD4+ helper inducer T lymphocytes.