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Biomedical subjects

M Cembrzyńska-Nowak

Publications and source records attributed to M Cembrzyńska-Nowak.

At least 19 recordsLinked to original sources
PubMed2002

Relevance of the selected cytokine release (TNF-alpha, IL-6, IFN-gamma, and IFN-alpha) to the exacerbation of bronchial asthma from airway mycotic infections. Predominant role of TFN-alpha?

Airway fungal infections are often associated in asthmatics with the exacerbation of asthma symptoms. However, the pathomechanism of this phenomenon has not been fully understood. The aim of our study was to assess whether antimycotic treatment can influence the capacity of bronchoalveolar (BAL) leukocytes to release proinflammatory cytokines, which could contribute to increase in asthma severity. Ten patients with bronchial asthma complicated by airway fungal infections (Candida albicans and/or Aspergillus fumigatus) were included in the study. Seven asthmatics were treated with systemic and inhaled corticosteroids, whereas the remaining three with inhaled ones only. All subjects underwent several courses of therapy with antibiotics due to respiratory infections. BAL leukocytes obtained from the patients were cultured in the absence or presence of lipopolysaccharide E.coli (LPS) or Newcastle disease virus (NDV). The BAL procedure and measurement of the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (II-6), interferon-gamma (IFN-gamma), and interferon-alpha (IFN-alpha) by specific bioassays were performed twice: before antimycotic treatment and after 3 weeks of therapy with 8 mg of nebulized fluoconazole and 400 mg of oral ketoconazole per day. The elimination of fungi from respiratory tract resulted in an apparent clinical improvement. This coincided with diminished production of TNF-alpha in response to LPS and the production of IFN-alpha in response to NDV, which were initially high and subsided significantly after antimycotic therapy (p = 0.035, and 0.011, respectively). Such changes were not observed in the case of IFN-gamma and IL-6. This may suggest that TNF-alpha as well as IFN-alpha are secreted by fungi-prestimulated leukocytes from the lower respiratory tract and may be involved in the processes of exacerbation of asthma complicated by fungal infections. Further analyses of relationships between changes in cytokine levels and clinical parameters indicated that IFN-alpha seems to be of particular interest in fungal stimulation of asthma.

Adult↗
PubMed2001

[The ability to produce nitric oxide by leukocytes in whole blood of children with recurrent urinary tract infections].

We examined 20 children in age from 6 till 18 years old with recurrent urinary tract infection (rUTI). The control group were 15 healthy volunteers in age from 19 till 23 years old. In all cases nitrogen oxide concentration was designated in supernatant of 48 hours leukocytes culture with using colorimetric method with Griess reagent described by Ding. The spontaneous and LPS stimulated ability to nitrogen oxide production in full blood was estimated. The nitrogen oxide index was counted from the difference of concentration of inducated and stimulated nitrogen oxide. The defective response of the leukocytes of full blood to LPS-stimulation for nitrogen oxide productionin aggravation also in remission in children with rUTI and with rUTI in age till 5 years old and above 5 years old comparing to healthy ones.

Adolescent↗
PubMed2000

The contribution of endotoxins present in the respiratory tract to overproduction of nitric oxide associated with impaired interleukin 6 release in bronchoalveolar leukocytes from lung cancer patients.

The purpose of the study was to assess the relation between the levels of endotoxins circulating in airways of patients with lung cancer and the ability of bronchoalveolar lavage (BAL) leukocytes for ex vivo release of nitric oxide (NO) and interleukin 6 (IL-6) and for in vitro lipopolysaccharide (LPS)-induced production of the mediators. Leukocytes isolated from the BAL of 11 patients and from 5 healthy individuals were cultured in the absence or presence of LPS(E. coli). The levels of endotoxins in the BAL fluids (BALF) and the amounts of NO released ex vivo from unstimulated cells from the patients were highly (p = 0.0025) elevated in comparison with those from healthy individuals. The release of NO was significantly correlated (R(S) = 0.638, p = 0.047) with the levels of endotoxins in BALF. In contrast, production of IL-6 remained very low and a negative correlation (R(S) = -0.623, p = 0.0542) was observed between the amounts of NO and IL-6. It was also found that, in response to LPS, bronchoalveolar leukocytes from patients with lung cancer express a reduced capacity for in vitro production of NO and IL-6. Our data suggest that, in patients with lung cancer, the activation of BAL cells by endotoxins circulating in the airways may contribute, at least in part, to overproduction of spontaneous NO and, subsequently, the NO may reduce IL-6 production. Moreover, the exposure in vivo of the BAL cells to LPS renders them unable to respond to the second signals.

Adult↗
PubMed1998

TNF-alpha, IL-6 and IFN-gamma secreted by bronchoalveolar leukocytes isolated from patients with bronchial asthma, complicated by fungal airways infections.

It is widely known that fungal airways infections may deteriorate the course of bronchial asthma. The mechanism of the phenomenon is still unclear. The aim of our study was to assess the effect of fungal infections on the secretion of selected cytokines by bronchoalveolar leukocytes. Five patients (group FA) with bronchial asthma and Candida albicans or Aspergillus fumigatus airways infections (confirmed by bronchoscopy and culture) were included in the study. All of them were on the chronic treatment with corticosteroids (10-20 mg of prednisone per day) and underwent several courses of therapy with antibiotics. The control groups comprised 5 previously untreated asthmatics without bronchial colonization with fungi (group A) as well as 5 healthy volunteers (group H). Leukocytes were isolated from bronchoalveolar lavage fluid (BALF) and cultured in the presence or absence of cytokine inducers such as phytohemagglutin L (PHA), lipo-polysaccharide (LPS) from E. coli. The activity of TNF-alpha, IL-6 and IFN-gamma were measured in the BAL cell culture supernatants by using specific bioassays. In comparison with healthy controls the spontaneous or induced secretion of cytokines were significantly augmented in patients from group A. In contrast the asthmatics who represented group FA demonstrated normal levels of spontaneous cytokine secretion. However, the tendency to increase LPS and PHA-induced production was observed in BAL leukocytes from the patients. The above results support the view that beneficial effect of corticosteroid treatment in bronchial asthma may act, at least in part, by inhibition of the high spontaneous secretion of proinflammatory cytokines. Nevertheless, fungal airways infections may lead to increase of LPS- or PHA-induced production of TNF-alpha, IL-6 or IFN-gamma (despite prednisone therapy) by prestimulation of the BAL cells with fungi.

Adult↗
PubMed1998

Exogenous interleukin 2 regulates interleukin 6 and nitric oxide but not interferon gamma and tumor necrosis factor alpha production in bronchoalveolar leukocytes from patients with small cell lung cancer.

The relationship and in situ interactions between interleukin 2 (IL-2)-regulated mediators remain unclear, particularly in lung cancer model. The purpose of the present study was to determine in vitro effect of IL-2 on the secretory activity of bronchoalveolar leukocytes from 11 patients with previously untreated small cell lung cancer (SCLC) and 9 patients with non-small cell lung cancer (NSCLC). Control group (n = 6) comprised patients who underwent diagnostic investigations and were free of any clinical or radiographic evidence of lung diseases. IL-2-induced secretion of mediators was compared with that following stimulation with lipopolisaccharide (LPS; 5 micrograms/ml) or Newcastle disease virus (NDV; 640 HU/ml). Obtained from bronchoalveolar lavages (BAL) cells were cultured for 24-48 h in the presence or absence of inducers. The levels of cytokines were determined in BAL cell supernatants by bioassays. Nitric oxide (NO) was estimated by colorimetric method in Griess reaction. Compared with normal controls, the spontaneous secretion of the above mediators excluding IFN-gamma in BAL cultures from NSCLC group was elevated by up to 20-30-fold and further increase was observed after stimulation with LPS. However, very low secretion of cytokines and NO was found in BAL leukocyte cultures activated by IL-2. In contrast, the cells obtained from SCLC group produced little detectable levels of TNF-alpha (median 12.0, range 3-45 U/ml), IFN-gamma (median 3, range 3-12 U/ml) and IL-6 (median 15, range 6-45 U/ml) in response to LPS and interferons, mainly IFN-alpha; (median 3, range 3-12 U/ml) in response to NDV. Although, upon IL-2-stimulation was observed only noteworthy production of IL-6 (median 405, range 45-1215 U/ml). IL-2-induced secretion of IL-6 was accompanied by up to 5-fold augmented secretion of NO in comparison with NSCLC group and healthy controls. These observations suggest that BAL cells from patients with lung cancers express a selective secretory activity and that IL-2 is an important regulatory factor of secondary production of IL-6 and NO. Utilization of IL-2 in therapeutic strategy in SCLC can lead to alterations in synthesis/release of biologically active IL-6 and NO that may contribute to the clinical settings.

Adult↗
PubMed1997

Modulation of cytokine production by a selenoorganic compound (AE-22) in hyperreactive or hyporeactive bronchoalveolar leukocytes of asthmatics or lung cancer patients.

We have found that many synthetic selenoorganic compounds, including ebselen, have immunotropic activity. These studies were designed to assess the effect of the analog of ebselen bis[2-pyridyl (2-carbamoyl) phenyl]diselenide (AE-22) on human leukocytes that may express various activation states. The cells were obtained from bronchoalveolar lavage (BAL) cells of patients with various inflammatory lung diseases. The AE-22-treated BAL cells from patients with bronchial asthma (n = 6) and with small cell lung cancer (SCLC) (n = 6) were compared with these in the peripheral blood leukocytes (PBL) from the same donors. The control group comprised 5 patients who underwent diagnostic examination and were free of any cancer or concomitant diseases. Secretion of TNF-alpha, IL-6, and IFN-gamma was considered as a marker of BAL or PBL cell activation. Different response of the cells and various effects of AE-22 were observed in relation to the origin and functional state of leukocytes. It was established that AE-22 can induce TNF-alpha, IL-6, and IFN-gamma in a dose-dependent manner in BAL cells and PBL isolated from healthy individuals. However, BAL cells were found to be less reactive than PBL as cytokine producers. In contrast, AE-22 had no effect on BAL cells obtained from patients with lung cancer, which were found to be hyporeactive to phytohemagglutinin and bacterial lipopolysaccharide and did not produce TNF-alpha, IL-6, or IFN spontaneously. The spontaneous release of cytokines by BAL cells from bronchial asthma patients, but not by PBL from the same individuals, was significantly (p < 0.01) higher than that from the cultures of healthy control subjects. The high secretion of cytokines by the locally activated BAL cells was significantly (p < 0.01) reduced after administration of AE-22. The results suggest that AE-22 has immunomodulatory activity. AE-22 can downregulate the hyporeactive BAL cells from asthmatics, but it appears to be inactive in BAL cells of cancer patients who can tolerate the cytokine inducers.

Adult↗
PubMed1996

[Effect of post-trauma endotoxemia on production of IL-1 beta in burn patients].

Thermal injury-associated endotoxemia affects the in vitro induction of interleukin-1 beta (IL-1 beta) synthesis by inflammatory stimuli. Pathophysiological effects related to the interaction between bacterial endotoxins and human monocytes/marcrophages are complex and may have significant impact on defense response of burn host. Therapeutic approaches in critically ill burn patients should be considered in the context of the overall biological activity of endogenous mediators of immune and inflammatory reactions involved.

Burns↗
PubMed1992

Effect of natural and synthetic immunomodulators on the synthesis of interferon by peritoneal cells of mice.

The effect of different natural and synthetic immunomodulators on the spontaneous interferon (IFN) synthesis by freshly isolated resident peritoneal cells of BALB/c, NZB and C3H mice was investigated. Actinomycetal glycolipids isolated from Curtobacterium betae, Faenia rectivirgula, Rothia dentocariosa and Saccharopolyspora hirsuta at the concentration 1-20 micrograms/ml were found to potentiate the IFN synthesis by the peritoneal cells of BALB/c mice. Similar results were obtained when dsRNA, LPS of Shigella sonnei and lipid A isolated from the LPS were used. The effect of potentiation of the physiological IFN production by the immunomodulators was observed also in the cells of C3H and NZB mice. In contrast, the inhibition of the IFN synthesis was observed when the peritoneal cells of BALB/c and NZB mice were treated with imuthiol at concentration 0.1-10 micrograms/ml. Thymomodulin (TFX-Polfa) at concentration of 1-100 micrograms/ml had no effect on the spontaneous IFN production.

Adjuvants, Immunologic↗
PubMed1992

Human lymphoid target cells for the cytokine-inducing seleno-organic compounds.

Several seleno-organic compounds including ebselen are known as antiinflammatory and antioxidant agents. They also have glutathione peroxidase-like activity and are inhibitors of leukotrienes and prostaglandins. We have recently discovered that these drugs are inducers of cytokines, mainly interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) and mitogenic interleukins in human peripheral blood leukocytes (PBL) but not in the mouse or rat lymphoid cells. We described a production of IFN-gamma and TNF-alpha by various subsets of PBL stimulated with 2-phenyl-1,2-benzisoselenazol-3(2H)-one (ebselen) or bis [2-(N-phenyl-carbamoyl)]phenyl diselenide. IFN-gamma was produced mainly by E-rosette positive lymphocytes. However, the presence of monocytes was required for the optimal production of IFN-gamma. Also soluble mediators released by monocytes enhanced IFN-gamma synthesis. On the other hand, TNF-alpha was produced mainly by the adherent monocytes. Its synthesis was enhanced by the addition of T or B lymphocytes or conditioned medium from the culture of the stimulated lymphocytes. The relative concentrations of the subsets of lymphocytes or monocytes was important for the maximum production of both IFN-gamma and TNF-alpha. High concentration of lymphocytes inhibited the cytokine production.

Adjuvants, Immunologic↗
PubMed1990

Hyporesponsiveness of human alveolar leukocytes to interferon-alpha and interferon-gamma inducers.

Leukocytes were obtained from bronchoalveolar lavages (BAL) of 36 patients including 10 with lung cancer, 15 with inflammatory lung diseases and 11 healthy control patients undergoing diagnostic investigation. The entire alveolar cell population responded weakly to the classic interferon (IFN) inducers: Newcastle disease virus (NDV), phytohemagglutinin (PHA) and lipopolysaccharide (LPS). This refers mainly to normal healthy volunteers. Alveolar leukocytes from patients with inflammatory lung diseases and nonsteroid treated lung cancer responded better to the interferon inducers than did cells from other patients. The IFN-alpha or IFN-gamma response of whole blood leukocytes to the same inducers was 10 to 100-fold higher than that of the alveolar cells. Alveolar macrophages from 6 healthy individuals and 3 patients with inflammatory lung disease were cultured in vitro for 6 days. The IFN response to inducers appears to depend on the origin of the cultured cells. It increased in the initially hyporeactive macrophages from healthy subjects and decreased in the relatively reactive cells from the patients with inflammatory lung diseases. We suggest that the hyporeactivity to IFN induction is a physiological state of the alveolar leukocytes which are a specialized cell population having constant exposure to inhaled agents such as dust, smoke, microorganisms and their by-products. The hyporesponsiveness to IFN induction of the alveolar cells may have an important physiological role in protecting lungs against hyperproduction of cytokines involved in the inflammatory and allergic reactions.

Adult↗
PubMed1989

Different antiviral activity and cell specificity of interferon preparations produced by mouse peritoneal cells at 37 degrees C and at 26 degrees C.

Three sublines of mouse L cells and mouse embryo fibroblasts were used for determination of the antiviral activity of mouse interferons produced by nonadherent peritoneal exudate cells incubated either at 37 degrees C or at 26 degrees C. IFN produced at 37 degrees C or at 26 degrees C had the same antiviral activity in L Borgen, L929 cells. However, in MEC IFN-37 degrees had relatively higher activity than IFN-26 degrees. Of the interferon investigated only IFN-37 degrees exhibited antiviral activity in the established line of rat kidney cells. The IFN preparations showed no activity in the human and chicken cells. The studies on the sensitivity of viruses to both forms of IFN revealed that EMC and VSV viruses were equally sensitive to IFN-26 degrees C. However, the replication of EMC virus was more strongly inhibited by IFN-37 degrees than the multiplication of VSV virus.

Animals↗
PubMed1989

Effect of temperature on interferon production in mouse lymphocytes.

Interferon production by NDV-stimulated mouse cells was tested at various temperatures. The peritoneal non-adherent lymphocytes, adherent macrophages, mouse embryonic fibroblasts and L929 cells were used. Only lymphocytes produced two types of interferons depending on the temperature of incubation. Multifold stimulations of lymphocytes with NDV with parallel alterations of the temperature of incubation revealed that as early as after the first stimulation, they achieved the state of tolerance and stopped producing interferon even after repeated inductions or temperature alterations. It was also noted that the temperature of cell incubation determines the production of two types of interferon as soon as interferon appeared in the culture fluid.

Animals↗
PubMed1988

Investigation on extracellular slime from Pseudomonas aeruginosa as interferon inducer in mice.

The investigation concerns interferon (IFN) production in the sera and spleens of 129/Ao/Boy mice induced with Pseudomonas aeruginosa slime extract. Interferon was present in the serum as early as 2 h after i.v. and i.p. injection of the immunogenic dose of the slime - 100 micrograms/mouse. Likewise, in the spleen the same dose induced interferon production at the second hour after its administration. In the spleen interferon was synthetized longer, even up to 7 days. On the other hand, it disappeared from the serum after 24 h. In vitro investigations on interferon induction in peritoneal cells and spleen revealed that after slime extract stimulation, only non-adherent cells are capable of IFN production; while adherent cells are not. Interferon synthesis in peritoneal cells in vitro was much enchanced if for the experiments, cells isolated 2 - 4 h after i.v. administration of mice with Ps. aeruginosa slime extract, were used. Besides, the stimulatory effect of the extract on interferon production was well marked in the Newcastle virus-induced peritoneal cells. For comparison, interferon obtained after induction with slime extract in vivo (in the serum) and in vitro (in peritoneal cells) was tested for its properties. The interferons although both acidstable, displayed significant differences. IFN obtained in vitro from peritoneal cells culture appeared thermolabile and susceptible for neutralization with gamma-globulin of rabbit serum against interferon from Newcastle virus-induced L929 cells (anti-MuIFN alpha/beta). IFN from serum was thermostabile, undergoing only slight neutralization with anti-MuIFN alpha/beta globulin.

Animals↗
PubMed1986

Interferon production in Propionibacterium acnes treated mice.

Interferonogenic properties of Propionibacterium acnes (PA) was studied in vivo and in vitro using CBA, BALB/c and 129AoBoy strains of mice. IFN was induced only in CBA strain after i.v. PA injection. BALB/c and 129AoBoy mice did not produce IFN. In the sera of CBA mice, obtained after i.p. injection of PA, interferon was not found. However, spleen cells of these mice produced IFN beginning from the 3rd day after injection. This interferon response lasted until the 10th week. Furthermore, in vivo studies showed enhancement effect of PA i.p. injection on IFN synthesis when NDV was introduced i.v. as inducer. The increased interferon level was also observed in the peritoneal cells isolated from PA--pretreated mice, induced in vitro with NDV or PA.

Animals↗
PubMed1986

Interferons from mouse lymphocytes produced at various temperatures (26 degrees C and 37 degrees C).

The study concerns the synthesis and properties of interferons induced at various temperatures (26 degrees C and 37 degrees C) with Newcastle Disease Virus (NDV) in mouse lymphocytes from peritoneal cavity. The results obtained revealed differences in the kinetics of their production. IFN synthesis at 37 degrees C proceeded fast while at 26 degrees C this process was slower and longer lasting. Besides, it was shown that both interferons differ in antigenic properties, molecular weight--IFN (37 degrees C)--26,000, IFN (26 degrees C)--40,000, and resistance to temperature (56 degrees C).

Animals↗
PubMed1984

Spontaneous interferon in viral infection in mice.

Experimental infection of Balb/c mice with EMC virus (Co1MM strain) suppresses the process of spontaneous interferon (IFNsp) synthesis, regardless of the dose of virus used. Small doses of Co1MM virus which cause neither virus replication nor interferon induction in the animal organs, inhibit the production of spontaneous interferon as early as 1 h after infection. This inhibition is not permanent and is followed by a return to the norm and in some cases even by intensification of spontaneous interferon synthesis.

Animals↗
PubMed1983

Human interferons and their purification.

The present paper describes briefly the procedure used in our laboratory for the preparation of HuIFN-alpha. Induction of interferon was carried out in the suspension of human leukocytes from peripheral blood, using Newcastle virus as inducer. The optimal conditions to produce interferon were established in the media with and without serum. Moreover, the work reports the results of studies on the purification of HuIFN-alpha and HuIFN-beta interferons.

Cells, Cultured↗