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Helicobacter pylori antigens, acetylsalicylic acid, LDL and 7-ketocholesterol - their potential role in destabilizing the gastric epithelial cell barrier. An in vitro model of Kato III cells

100%

Gajewski A. , Mnich E. , Szymanski K. , Hinc K. , Obuchowski M. , Moran A. P. , Chmiela M.

Acta Biochimica Polonica

2016

tom 63

nr 1

Helicobacter pylori lipopolysaccharide activity in human peripheral blood mononuclear leukocyte cultures

84%

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.

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

84%

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.