Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
Polish version English version Language
enabled [disable] Abstract
Number of results

Results found: 12

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

Search:
in the keywords:  ASTHMA
help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
1

All roads lead to Rome: pathways of NKT cells promoting asthma

100%
Jinquan T., Li W., Yuling H., Lang C.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
vol. 54
|
issue 5
335-340
EN
NKT cells are the prominent manipulator in asthma development. Asthmatic NKT cells migrate from thymus, spleen, liver and bone marrow into blood vessels, and then concentrate in airway bronchi mucosa. This recruitment is dependent on high expression of CCR9 and engagement of CCL25/CCR9. NKT cells promote asthma in two different pathways. One is an indirect pathway. NKT cells contact with CD3+ T cells and induce them secreting large quantity of Th2 cytokines (IL-4, IL-13), which requires the participation of dentritic cells and the synergic signaling of CCL25/CCR9 and CD226. The other is a direct pathway. Circulating asthmatic NKT cells selectively highly express Th1 cytokines . Once reached airway epithelium, most NKT cells shift to Th2-bias, highly expressing IL-4, IL-13, but not IFN-alpha. Both pathways lead to airway hyperresponsiveness and inflammation, asthma development. Comparing to the well documented suppressive regulatory T cells, CD4+CD25+ T cells, NKT cells perform as a novel active regulator in asthma. These recent understanding of NKT cells performance in the development of asthma might unveil new therapy targets and management strategies for asthma.
2

Expression of naive/memory (CD45RA/CD45RO) markers by peripheral blood CD4+ and CD8+ T cells in children with asthma

100%
Machura E., Mazur B., Pieniazek W., Karczewska K.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56
|
issue 1
55-62
EN
Introduction: The role of CD4+ T cells in the immunopathogenesis of asthma is well documented. Little is known about the role of CD8+ T cells. The aim of this study was to assess peripheral blood subsets of CD4+ and CD8+ T cells expressing naive/memory markers (CD45RA+/RO+) and the activation marker (CD25+) in children with allergic asthma. Materials and Methods: Peripheral blood mononuclear cells were isolated from children with allergic asthma and healthy children. T cell subsets were analyzed by flow cytometry for the expressions of CD45RA, CD45RO, and CD25. In this study, some differences in the memory compartment of peripheral blood T cells between asthmatic children and healthy controls were detected. Results: The absolute number of CD8+ T cells expressing CD45RO was significantly elevated and the percentages of CD3+ T cells expressing activation marker CD25 and of CD4+ T cells expressing memory marker CD45RO were significantly lower in children with asthma compared with controls. No correlation was found between severity of asthma and peripheral blood lymphocyte subsets. Conclusions: There were some differences in the memory compartment of peripheral blood T cells between asthmatic children and healthy controls. The increase in the number of CD8+ T cells expressing the memory marker (CD45RO) in children with allergic asthma may indicate that CD8+ T cells play a role in the pathogenesis of asthma.
3

Effect of recombinant IFN-gamma on IgE-dependent leukotriene generation by peripheral blood leukocytes in patients with pollinosis and asthma

100%
Krasnowska M., Medrala W., Malolepszy J., Krasnowski R.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 4
287-292
EN
Interferon gamma (IFN-gamma) is considered one of the causative and intensifying factors in inflammation. The reaction to allergens releases IFN-gamma, an immunomodulatory cytokine known to inhibit IgE synthesis and Th cell proliferation. The aim of the study was to evaluate the influence of IFN-gamma on leukotriene (LT) release in vitro, from human leukocytes of atopic patients with pollinosis and asthma. Thirty-eight patients were enrolled in the study: 15 with pollinosis and 23 asthmatics. In the presence of IL-3, leukocytes were stimulated with specific allergens. Other samples of leukocytes were preincubated with different concentrations of IFN-gamma for 15 min before allergen stimulation. The concentration of LT in supernatants was measured according to the CAST-ELISA procedure. We stated that IFN-gamma had significantly diminished LT release in a dose-dependent mode from the leukocytes of pollinotics. IFN-gamma did not change LT release in the asthmatic group, although, in leukocytes the small and medium basic production of LT, IFN-gamma caused a statistically significant fall in LT generation.
4

Bronchial hyper-responsiveness, subepithelial fibrosis, and transforming growth factor-beta1 expression in patients with long-standing and recently diagnosed asthma

100%
Tomkowicz A.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56
|
issue 6
401-408
EN
Chronic inflammation in asthmatic airways leads to bronchial hyper-responsiveness (BHR) and the development of structural changes. Important features of remodeling include the formation of subepithelial fibrosis due to increased collagen deposition in the reticular basement membrane. Transforming growth factor (TGF)-beta might be a central mediator of tissue fibrosis and remodeling. Materials and Methods: Immunohistochemistry was used to measure collagen III deposition and TGF-beta1 expression in biopsies from patients with long-standing asthma treated with inhaled corticosteroids, patients with recently diagnosed asthma, and control subjects. Computer-assisted image analysis was used to evaluate total basement membrane (TBM) thickness. Asthmatics, particularly those with long-standing asthma, had thicker TBMs than healthy subjects. Collagen III deposition was comparable in the studied groups. BHR was not correlated with features of mucosal inflammation and was lower in steroid-treated patients with long-standing asthma than in subjects with newly diagnosed asthma untreated with steroids. Epithelial TGF-beta1 expression negatively correlated with collagen III deposition and TBM thickness. Conclusions: The study showed that TBM thickness, but not collagen III deposition, could be a differentiating marker of asthmatics of different disease duration and treatment. The lack of correlation between BHR and features of mucosal inflammation suggests the complexity of BHR development. Corticosteroids can reduce BHR in asthmatics, but it seems to be less effective in reducing subepithelial fibrosis. The role of epithelial TGF-beta1 needs to be further investigated since the possibility that it plays a protective and anti-inflammatory role in asthmatic airways cannot be excluded.
5

Nitric oxide (NO) in the pathophysiology of asthma and interstitial lung diseases

100%
Kasperska-Zajac A., Rogala R. B., Rogala B., Kasperka-Zajac A.
|
|
vol. 55
|
issue 4
525-540
EN
NO is an important mediator of immune and inflammatory responses. NO is produced from L-arginine by three isoforms of nitric oxide synthase (NOS), neuronal (nNOS; NOS1), endothelial (eNOS; NOS3) and inducible (iNOS). Exhaled NO has been shown to be increased in asthma and has been put forward as a marker of airways inflammation. Moreover, increased production of NO and peroxynitrite may be responsible for the oxidative damage and fibrosis seen in interstitial lung diseases. The present review focuses on clinical and laboratory studies that are aimed at identifying the role of NO in the physiopathology of these disorders.
6

GM-CSF regulation in eosinophils

100%
Esnault S., Malter J. S.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
|
vol. 50
|
issue 2
121-130
EN
Allergic asthma is characterized by a temporally and quantitatively inappropriate immunologic response. One of hallmarks of this response is the accumulation of eosinophils in the airway and lung parenchyma, which results in bronco-constriction, lung damage and ultimately fibrosis. GM-CSF plays a pivotal role in this process by modulating eosinophil function and survival. In this review, we discuss the effects and molecular regulation of GM-CSF secretion by eosinophils. Recent data demonstrate activated eosinophils release small amounts of anti-apoptotic GM-CSF by stabilizing its coding mRNA.
7

Nitric oxide production by pulmonary leukocytes from induced sputum in patients with asthma and its effect on epithelial cell viability

88%
Bienkowska-Haba M., Liebhart J., Cembrzynska-Nowak M.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
vol. 54
|
issue 3
201-207
EN
Nitric oxide (NO) is one of many factors potentially involved in lung remodeling in asthma. The aim of the study was to assess the effect of pulmonary leukocytes from patients with bronchial asthma on alveolar epithelial cell damage in relation to NO production. Materials and Methods: Induced sputum samples were obtained from 25 patients with bronchial asthma and 10 healthy volunteers. Twelve asthmatics were on inhaled corticosteroid treatment and 13 were corticosteroid free. Type II-like alveolar epithelial (A549) cells were cultured for 48 h in the presence of cell-free media from a 24-h culture of leukocytes obtained from the induced sputa (IS-Su). The level of NO was measured in supernatants from the cell cultures and the viability of the A549 cells was established. Results: The levels of NO in IS-Su from corticosteroid-free asthmatics were significantly higher (p=0.001) than those in IS-Su from healthy controls. Furthermore, NO production by A549 cells exposed to IS-Su from steroid-free asthmatics (group A) was significantly higher than that from asthmatics on corticosteroid therapy (group cA) as well as from healthy controls (p=0.01 and p=0.001, respectively). Lower viability of the epithelial cells exposed to IS-Su was observed in group A compared with controls (median: 72% vs. 97.5%; p<0.001). In addition, a negative correlation (RS=?0.706, p<0.001) was found between the levels of NO produced by pulmonary leukocytes and the viability of epithelial cells. Conclusions: The results suggest that in the course of asthma, pulmonary leukocytes may interact with alveolar epithelial cells by inducing an excessive production of NO which, in turn, may contribute to epithelium impairment.
8

Expression profile analysis of human peripheral blood mononuclear cells in response to aspirin

88%
Choi S., Park H.-S., Cheon M. S., Lee K.
|
EN
Aspirin is a popular nonsteroidal anti-inflammatory drug, but some patients suffer from hypersensitivity to it. This prompted us to identify the factors or molecules related to these responses. A commercially available DNA microarray was used to study changes in gene expression in human peripheral blood mononuclear cells (PBMCs) after aspirin treatment. The PBMCs were collected from a patient with aspirin-intolerant asthma and one normal healthy control. We identified 61 and 107 genes respectively induced and repressed by aspirin treatment in the PBMCs derived from the normal control. In the patient showing aspirin-induced asthma responses, 31 genes were up-regulated and 6 were down-regulated after aspirin treatment. Among these, 1 gene was expressed with the same pattern in the control and the patient. In contrast, 19 genes showed different expression patterns, and it turned out that most of them were involved in immune responses, cell growth/proliferation, transcription/ translation, and signaling pathways. These results show the molecules involved in hypersensitivity to aspirin and may lead to a better understanding of adverse responses to aspirin. Furthermore, they can provide clues for identifying novel therapeutic and/or preventive molecular targets of the adverse effects of aspirin.
9

Genetic polymorphism of beta 2-adrenoceptor and its role in pathology

88%
Woszczek G., Kowalski M. L.
|
|
vol. 55
|
issue 1
37-51
EN
A few polymorphic loci has recently been identified in the beta 2-adrenoceptor gene that significantly influence receptor expression and its functions. Gene structure, regulation of the receptor expression and functions in regards to genetic polymorphisms and pathology are described.
10

Low molecular weight protein tyrosine phosphatase and human disease: in search of biochemical mechanisms

88%
Bottini N., Bottini E., Gloria-Bottini F., Mustelin T.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
|
vol. 50
|
issue 2
95-104
EN
A major challenge in the post-genomic era is to identify the physiological function of genes and elucidate the molecular basis for human disease. Genetic polymorphisms offer a convenient aveune for these efforts by providing evidence for the involvement of a given gene in human pathophysiology. Here we review the current evidence linking the low molecular weight protein tyrosine phosphatase (LMPTP) to several common diseases, including allergy, asthma, obesity, myocardial hypertrophy, and Alzheimer's disease. Based on the know effects of the genetic polymorphisms on the alternative mRNA splicing and enzyme levels of LMPTP, we discuss the possible molecular mechanisms of LMPTP involvement in these diseases.
11

A review of asthma genetics: gene expression studies and recent candidates

75%
Malerba G., Pignatti P. F.
Journal of Applied Genetics
|
2005
|
vol. 46
|
issue 1
93-104
EN
Recent evidence indicates an important role of inflammation pathways, airways remodeling and epithelium activation in asthma genetics. In particular, transcriptome studies have detected differentially expressed genes involved in eosinophil apoptosis, the arginase pathway, response to allergens or interleukins, and to inhaled corticosteroids. Candidate gene and genome wide studies have localized genetic regions involved in the disease, such as the A1AR and CLCA1 genes (chromosome 1), IL-1RN and DPP10 (2q14), HLA-G and TNF- (6p21), GPRA (7p14), FcRI and GSTP1 (11q13), NOS1, IFNG, STAT6, VDR, and other genes (12q13-26), PHF11 and flanking genes (13q14), AACT and PTGDR (14q), and ADAM33 (20p13). The role of these and other genetic determinants has to be confirmed in future, preferably longitudinal, studies.
12

Role of ADRB2 gene polymorphism in asthma and response to beta2-agonists in Polish children

75%
Szczepankiewicz A., Breborowicz A., Sobkowiak P., Kramer L., Popiel A.
Journal of Applied Genetics
|
2009
|
vol. 50
|
issue 3
275-281
EN
The aims of this study were: (1) to find associations of asthma with single-nucleotide polymorphisms (SNPs) within the ADRB2 gene: Arg16Gly, Gln27Glu,-1023 G/A, ?367 T/C,-47 C/T ; (2) to define linkage disequilibrium in the gene region, basing on the analyzed SNPs; and (3) to analyze the importance of ADRB2 polymorphism for response to bronchodilator drugs in children diagnosed with bronchial asthma. We compared 113 asthmatic children and 123 healthy subjects from the Polish population. Genotyping was performed by PCR-RFLP. We found an association of the A allele of ?1023A/G ADRB2 polymorphism with asthma (P = 0.024). No significant associations with other SNPs were detected. Moderate linkage was found between Gln27Glu and -47C/T polymorphisms in linkage disequilibrium analysis (D' = 0.85, r2 = 0.429, LOD = 31.97). No significant differences were found in haplotype frequencies in comparison to the control group, implicating that they are not associated with susceptibility to asthma in the analyzed population. There was no significant correlation between the analyzed SNPs of the ADRB2 gene and the response to beta2-agonists. This is the first report providing suggestive evidence for association of ?1023A/G ADRB2 polymorphism with an increased risk of asthma. The analyzed SNPs may not play a major role in response to beta2-agonists in asthmatic children.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.