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Biomedical subjects

Ryszard Rutkowski

Publications and source records attributed to Ryszard Rutkowski.

8 recordsLinked to original sources

[CD28 and CTLA-4 costimulatory molecules expression on T lymphocytes and NK cells in nonallergic bronchial asthma].

UNLABELLED: The aim of the study was to assess the role of costimulatory molecules in pathogenesis of nonallergic bronchial asthma. MATERIAL: The studied group consisted of 30 patients with nonallergic asthma, 24 with nonallergic asthma and recurrent respiratory tract infections and 20 healthy controls. RESULTS: In nonstimulated and lipopolysaccharide (LPS) stimulated cultures of control group the mean value of CD16+ + 56+ CD28+ subpopulation were significantly decreased compared to values in both types of asthma. Similar dependence was observed in cultures of asthmatic patients with infection and healthy person, stimulated with IL-15 and in CD4+CD28+, CD8 +CD28+ and NKCD28+ cultures from all studied groups, stimulated with LPS plus IL-15. In nonallergic asthma and infection asthma mean values of CD4 +CD152+ and CD16+ +CD56 +CD152+ from nonstimulated and IL-15 stimulated cultures were significantly increased compared to analogical values in control group. CONCLUSION: The results of our studies suggest that in nonallergic asthma the disturbed expression of costimulatory molecules may play an important role in pathomechanism of disease.

Adrenergic beta-Agonists↗

[Influence of treatment of inhaled corticosteroids on the function of the larynx in asthmatic patients].

UNLABELLED: The objective of the study was to examine influence of inhaled glycocorticosteroids on phoniatric function of the larynx in patients suffering from asthma. MATERIAL AND METHODS: Thirty minutes after the administration and long-term therapy effect of the inhaled glycocorticosteroids on local condition of the phoniatric organ was assessed in 15 patients with recently diagnosed bronchial asthma. The diagnostics of asthma included: subjective and objective examination, prick tests, spirometry, total IgE and histamine test for bronchial hyperactivity. Evaluation of voice function was implemented subjectively and objectively with use of videolaryngostroboscopy (VLSS). Acoustic assessment of voice was also performed. RESULTS: Administration of glycocorticosteroids as inhaled discs resulted in incidents of cough, mouth and throat dryness, sensation of polydipsia and skin inflammation around the mouth. Occasionally, hoarseness and discomfort in the larynx area were noted. On long-term administration, dysphonia, hoarseness and voice fatigue due to dysfunction of innermost larynx muscles, particularly vocal fold adductors. After 30 minutes of the glycocorticosteroid administration in patients with recently diagnosed asthma, irritation of the pharynx and larynx mucosa was recorded. CONCLUSION: The long-term treatment with inhaled glycocorticosteroids resulted in myopathy of proper muscles of the larynx.

Administration, Inhalation↗

[Vocal cord dysfunction or bronchial asthma?].

Vocal cord dysfunction (VCD) is a functional laryngeal dysfunction first described in the nineteenth century. It is quite frequent in patients with "refractory" asthma. It is very often treated as a steroid resistant asthma or exercise-induced bronchospasm, leading to unnecessary, aggressive asthma treatment and iatrogenic morbidity. Vocal cord dysfunction causes paradoxical adduction of vocal cords during the inspiratory phase of respiratory cycle, resulting in acute, episodic dyspnea not responding to typical antiasthmatic treatment. Laryngoscopy remains a gold standard for the diagnosis of vocal cord dysfunction. Additional pulmonary function tests may be useful. Fast and appropriate diagnosis of VCD is only possible with close collaboration of laryngologists and asthma specialists. The treatment of dyspnea attack in VCD involves psychological counseling, heliox application and sedative/anxiolytic agents. Long term treatment may include speech therapy, biofeedback, yoga and autohypnosis.

Asthma↗

[Methods of expired nitric oxide assessment in pulmonary diseases in children].

Assessment of exhaled nitric oxide (eNO) creates new diagnostic possibilities for evaluation of the inflammatory process especially in children, in whom not all of the contemporary methods of diagnosing respiratory tract diseases are applicable. eNO concentration can be measured in children of all age, including neonates. Direct assessment of eNO is possible with an on-line method, in which NO is directly exhaled into a chemiluminescence analyser. An off-line method is performed by exhalation into a collapsible bag of nonreacting material and analysing the collected air with appropriate analysers. eNO measurement is a non-invasive, repeatable, rapid and sensitive method, producing results even during measurement. Assessment of eNO in children may be used to quantify inflammation in asthma and other respiratory tract diseases specific for this age group. Monitoring of the therapy and response to the anti-inflammatory agents i.e. glucocorticosteroids and anti-leukotriene drugs can also be based on eNO measurement.

Breath Tests↗

[Analysis of intracellular cytokines IFN-gamma and IL-4 in peripheral blood T cells in children with bronchospastic reaction].

UNLABELLED: In the epidemiological study there was suggested that respiratory tract infections--were a strong risk factors for the beginning and development of bronchial asthma. The aim of the study was the evaluation of intracellular cytokine IL-4 and IFN-gamma on peripheral blood T subsets in children with atopic asthma (AA) and recurrent respiratory tract infection with bronchospasm (RRTI). METHOD: Peripheral blood T cells were stained with fluorescence-labelled antibodies specific for intracellular cytokines IFN-gamma and IL-4 and cell surface markers CD3, CD4 and CD8, and were subjected to flow-cytometric analysis. RESULTS: Comparing peripheral blood lymphocytes of atopic asthma patients with those of recurrent infections we found significantly more cells positive for IL-4 in asthma patients than in recurrent infection patients, both in the CD3+ subsets (p<0.03) and CD4+ subset (p<0.01). We have also found that percentage of CD4+ was significantly lower (p<0.007) and percentage of CD8+ cells was significantly higher (p<0.05) in RRTI group comparing to atopic asthma patients. In AA group there was a significant increase intracellular expression of IL-4 among the CD3+ (p<0.03) and CD4+ (p<0.01) subsets and no significant differences among CD8+ subset. In AA group there was a significant decrease ratio of IFN-gamma/IL-4 among all of the evaluated subsets. CONCLUSION: Basing oneself on these results we conclude that markers of atopy are: increased intracellular expression of IL-4 among CD4+ cells and decreased IFN-gamma.

Asthma↗

CD80 and CD86 expression on LPS-stimulated monocytes and the effect of CD80 and CD86 blockade on IL-4 and IFN-gamma production in nonatopic bronchial asthma.

CD80 and CD86 seem to play an important role in the allergen-induced secretion of interleukin (IL)-5 and IL-13. Up to now, the expressions of CD80 (B7.1) and CD86 (B7.2) on monocytes and the kinetics of the expression of these molecules on lipopolysaccharide-stimulated monocytes in nonatopic asthma have not been defined. Using monoclonal antibodies, we have compared the expressions of CD80 (B7.1) and CD86 (B7.2) on the monocytes of healthy persons and nonatopic asthmatic patients. We have also assessed the effect of CD80 and CD86 inactivation on IL-4 and interferon (IFN)-gamma production in nonatopic asthmatics and healthy subjects. We found that a low expression of CD80 (1.64 +/- 0.65 vs. 3.53 +/- 1.43%) and a moderate expression of CD86 (41.25 +/- 13.4 vs. 49.46 +/- 11.49%) on the studied monocytes were characteristic for asthma. In nonatopic asthma patients inactivation of CD80 or CD86 blockade significantly reduced IFN-gamma production by T lymphocytes (p < 0.02; p < 0.03). In both the studied groups, anti-CD80 antibodies did not diminish T lymphocyte production of IL-4. However, anti-CD86 antibodies significantly (p < 0.04) reduced the IL-4 concentration in culture supernatants. Our results confirm that both the CD80 and CD86 molecules play an important role in the maintenance and amplification of the inflammatory process. It suggests that in the inflammatory process that occurs in nonatopic bronchial asthma, Th1 as well as Th2 lymphocytes are equally important.

Adult↗

[The role of monocytes stimulated with LPS on CD69 expression in T lymphocytes of patients with non-atopic asthma].

CD69 molecule is the earliest antigen of T lymphocytes activation. We have studied the ex-pression of CD69 on LPS-stimulated T cells in nonatopic bronchial asthma. We have found that CD69 expression on freshly isolated peripheral blood T cells in nonatopic asthma patients was increased compare to control group (4.74 +/- 1.55/3.05 +/- 1.31) and the difference was statistically significant (p < 0.01). Monocytes added to nonstimulated T cell cultures increased 3-4 times the expression of CD69 and about 10-times in LPS-stimulated T lymphocytes.

Antigens, CD↗

[The effect of inactivation of co-stimulated particles B7.1 (CD80), B7.2 (CD86) on T lymphocyte activity].

We have studied the effect of CD80 (B7.1) and CD86 (B7.2) costimulatory molecules inactivation on IL-4 and IFN-gamma production by T lymphocytes. T cells were received from nonatopic asthmatic and healthy subjects. We have added anti-CD80 or anti-CD86 monoclonal antibodies to the monocyte/lymphocyte (1:5) cultures. In nonatopic asthma patients compare to control group inactivation of CD80 significantly reduced IFN-gamma production by T lymphocytes (2172/2368 pg/ml; p < 0.02). Blockade of CD86 decreased IFN-gamma production non-significantly (2858/3317 pg/ml; p < 0.3). In both studied groups anti-CD80 antibodies did not diminish T lymphocyte production of IL-4 (control: 630/725 pg/ml; nonatopic asthma: 718/742 pg/ml). Anti-CD86 antibodies reduced the IL-4 concentration in culture supernatants (630/523 pg/ml; 718/659 pg/ml), but the changes were nonsignificant.

Adult↗