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1

Choroba niedokrwienna serca a zakażenia bakteryjne Helicobacter pylori i Chlamydophila pneumoniae - rola białek szoku cieplnego i zjawisko mimikry antygenowej

100%
Matusiak A., Chmiela M.
Postępy Mikrobiologii
|
2013
|
tom 52
|
nr 3
2

Nowe stanowisko Anommatus duodecimstriatus (MULLER, 1821) (Coleoptera: Bothrideridae: Anommatinae) w Polsce

100%
Byk A., Matusiak A.
Wiadomości Entomologiczne
|
2014
|
tom 33
|
nr 3
3

Serological and cellular markers of host exposure to Campylobacter sp. in vitro studies

81%
Matusiak A., Puszer K., Szosland-Faltyn A., Chmiela M.
Postępy Mikrobiologii. Suplement
|
2017
|
tom 56
|
nr 1
4

Nowe stanowiska Hypocacculus rubripes (ERICHSON, 1834) i Saprinus georgicus MARSEUL, 1862 (Coleoptera: Histeridae) w Polsce

81%
Byk A., Gazurek T., Mazur S., Matusiak A.
Wiadomości Entomologiczne
|
2014
|
tom 33
|
nr 4
5

H.pylori surface antigens modulate the phenotype of circulating Natural Killer T cells

81%
Rudnicka K., Matusiak A., Chmiela M.
Postępy Mikrobiologii. Suplement
|
2017
|
tom 56
|
nr 1
6

Rola zakażenia Campylobacter jejuni w rozwoju Zespołu Guillaina-Barrego

81%
Walencka M., Matusiak A., Chmiela M.
Postępy Mikrobiologii
|
2018
|
tom 57
|
nr 3
7

CD25 (IL-2R) expression correlates with the target cell induced cytotoxic activity and cytokine secretion in human natural killer cells

81%
Rudnicka K., Matusiak A., Chmiela M.
Acta Biochimica Polonica
|
2015
|
tom 62
|
nr 4
8

Evaluating the efficacy of lactic acid bacteria and ozone disinfection to inhibit Campylobacter spp. growth in poultry meat

71%
Szosland-Faltyn A., Bartodziejska B., Laskarys J., Matusiak A., Chmiela M.
Postępy Mikrobiologii. Suplement
|
2017
|
tom 56
|
nr 1
9

Association of lipopolysaccharide-binding protein with CRP concentration, acute presentation and extent of coronary artery disease

61%
Rechcinski T., Matusiak A., Kurpesa M., Rudnicka W., Kasprzak J. D., Chmiela M.
Postępy Mikrobiologii. Suplement
|
2017
|
tom 56
|
nr 1
10

Antigen - specific lymphocyte proliferation as a marker of immune response in guinea pigs with sustained Helicobacter pylori infection

61%
Miszczyk E., Walencka M., Rudnicka K., Matusiak A., Rudnicka W., Chmiela M.
Acta Biochimica Polonica
|
2014
|
tom 61
|
nr 2
 Helicobacter pylori (H. pylori) bacteria are human pathogens causing symptomatic gastritis, peptic ulcer or gastric cancer. Little is known about the kinetics of immune responses in H. pylori infected patients because the initial moment of infection has not been identified. Various animal models are used to investigate the immune processes related to H. pylori infection. In this study we checked whether H. pylori infection in guinea pigs, mimicking natural H. pylori infection in humans, resulted in the development of specific immune responses to H. pylori antigens by measuring the proliferation of lymphocytes localized in mesenteric lymph nodes, spleen and peripheral blood. The maturity of macrophages and cytokines, delivered by monocyte-macrophage lineage or lymphocytes, were considered as mediators, which might influence the lymphocyte blastogenic response. The obtained results showed the activation of T cells localized in mesenteric lymph nodes by H. pylori antigens in H. pylori infected guinea pigs four weeks postinfection. The blastogenic activity of lymphocytes was shaped by their interaction with antigen presenting cells, which were present in the cell cultures during the whole culture period. Moreover, the balance between cytokines derived from adherent leukocytes including interleukin 8 - IL-8 as well as interferon gamma - IFN-γ, and transforming growth factor beta - TGF-β delivered by lymphocytes, was probably important for the successful proliferation of lymphocytes. The H. pylori specific lymphocytes were not propagated in peripheral blood and spleen of H. pylori infected animals. The modulation of immunocompetent cells by H. pylori antigens or their different distribution cannot be excluded.
11

Monocyte response receptors in BCG driven delayed type hypersensitivity to tuberculin

51%
Strapagiel D., Kasztalska K., Druszczynska M., Kowalewicz-Kulbat M., Vrba A., Matusiak A., Chmiela M., Rudnicka W.
Folia Histochemica et Cytobiologica
|
2008
|
tom 46
|
nr 3
353-359
12

Nowe stanowiska Limarus maculatus (STURM, 1800) (Coleoptera: Scarabaeidae: Aphodiinae) w Polsce

51%
Byk A., Gazurek T., Borkowski Z., Bidas M., Doktor D., Matusiak A., Mankina L., Plewa R.
Wiadomości Entomologiczne
|
2016
|
tom 35
|
nr 4
13

Autoantibodies against appetite-regulating peptides influence on ghrelin level in short children exposed to Candida albicans colonisation and Helicobacter pylori infection

51%
Czkwianianc E., Stawerska R., Smyczynska J., Hilczer M., Lewinski A., Socha-Banasiak A., Matusiak A., Chmiela M.
Postępy Mikrobiologii. Suplement
|
2017
|
tom 56
|
nr 1
14
Content available remote

Helicobacter pylori lipopolysaccharide activity in human peripheral blood mononuclear leukocyte cultures

51%
Grebowska A., Moran A. P., Bielanski W., Matusiak A., Rechcinski T., Rudnicka K., Baranowska A., Rudnicka W., Chmiela M.
Journal of Physiology and Pharmacology
|
2010
|
tom 61
|
nr 4
437-442
Helicobacter pylori (H. pylori) have been recognized as a major cause of chronic gastritis, gastric and duodenal ulcers and gastric cancer. Macrophages are the targets of lipopolysaccharide (LPS), which is a constituent of the outer membrane of Gram-negative rods. In this study we focused on a potential role of macrophages in the proliferation of human peripheral blood mononuclear leukocytes (PBML) in the milieu of H. pylori LPS and standard E. coli LPS. First, we found that H. pylori and E. coli LPS induced proliferation of total PBML (tPBML) from 5 out 21 healthy blood donors (LPS responders). In the LPS milieu, tPBML from the majority of volunteers (LPS non-responders) showed a significant decrease in the [3H]-thymidine incorporation as compared to tPBML in medium alone. The decreased cell proliferation was associated with a diminished metabolic activity of non-adherent lymphocytes. Then, non-adherent lymphocytes were stimulated with autologous macrophages pulsed with bacterial LPS. Still, the lymphocytes from the non-responders did not proliferate in the cultures with LPS exposed macrophages. In the group of LPS responders, the macrophages pulsed with H. pylori LPS significantly reduced the proliferation of non-adherent lymphocytes. The possible mechanism regulating the responses of PBML to bacterial LPS with an implication for the outcome of H. pylori infections is discussed.
15

Anti-phagocytic activity of Helicobacter pylori lipopolysaccharide [LPS] - possible modulation of the innate immune response to these bacteria

51%
Grebowska A., Moran A. P., Matusiak A., Bak-Romaniszyn L., Czkwianianc E., Rechcinski T., Walencka M., Planeta-Malecka I., Rudnicka W., Chmiela M.
Polish Journal of Microbiology
|
2008
|
tom 57
|
nr 3
The Helicobacter pylori infections are followed by an infiltration of the gastric mucosa by neutrophils and macrophages. Accumulation of phagocytes enables them to interact with H. pylori, but a great number of infected subjects cannot eradicate these bacteria. The H. pylori inhibits its own uptake by blocking the function of phagocytes. The anti-phagocytic mechanism depends on bacterial surface structures and the presence of the cag pathogenicity island (PAI). The role of H. pylori lipopolysaccharide (LPS), during phagocytosis of these bacteria is not clear. LPS may mediate direct bacteria/phagocyte interactions and it may also regulate antibacterial activity of the phagocytes. In this study we investigated the influence of H. pylori LPS on phagocytosis of these bacteria. The H. pylori LPS inhibited an ingestion of these microbes by human peripheral blood granulocytes. This was correlated with a diminished ability of phagocytes to reduce MTT-tetrazolium salt. The anti-phagocytic effect of H. pylori LPS was reduced by recombinant lipopolysaccharide binding protein (rLBP). It is possible that in vivo H. pylori LPS may diminish elimination of these bacteria from the gastric mucosa promoting an infection persistence. However, LBP may modulate the uptake of H. pylori due to neutralization of anti-phagocytic effect of its LPS.
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