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1

Occurrence of serum class G immunoglobulins interacting with specific antigens of Helicobacter pylori in patients with unstable coronary artery disease and in symptomless individuals

100%
Rechcinski T., Grebowska A., Kurpesa M., Rudnicka W., Krzeminska-Pakula M., Chmiela M.
Polish Journal of Microbiology
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2005
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tom 54
|
nr 3
An impact of Helicobacter pylori on the process of atherogenesis may be related to the intensity of humoral response against selected specific antigens of this bacteria. We performed serological studies in which the recognition of 7 selected antigens was possible. The investigated group consisted of 56 patients hospitalized due to unstable angina pectoris. The control group consisted of 29 symptomless volunteers. The levels of class G serum immunoglobulins interacting with glycine extract (GE) of H. pylori antigens were assessed by ELISA test in both groups. The same sera were tested by the Milenia blot H. pylori IgG system. In this assessment the presence of IgG antibodies interacting with antigens of molecular weight of 120, 87, 64, 35, 30, 26, and 20 kDa was estimated separately for every listed antigen. The results revealed significant differences between investigated groups in the prevalence of anti-GE IgG (unstable angina - 100% vs. controls - 60%) and in the level of such antibodies expressed as total optical density units - OD450 (6.1 ±3.0 vs. 3.4 ±3.0 respectively, p<0.05). However, anti-GE IgG detected in the sera of patients as well as controls reacted with similar frequency with selected H.pylori antigens: highly specific (120, 87, 64, 30 kDa) and specific (35, 26, and 20 kDa). We conclude, that although H. pylori infection is so common and mainly associated with gastroduodenal symptoms, it is also recognized by serological methods with high prevalence in patients with coronary artery disease, and less frequently in symptomless individuals. The humoral response against H. pylori in class G immunoglobulins in patients with unstable angina is characterized by higher levels of anti-H. pylori IgG but not by the higher prevalence of serum IgG interactions with the highly specific and specific H. pylori antigens. Such infection could be considered as a cofactor for atherogenesis by inducing strong humoral response against surface antigens of this bacteria.
2
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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
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2010
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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.
3

Natural mannose-binding lectin [MBL] down-regulates phagocytosis of Helicobacter pylori

84%
Strapagiel D., Grebowska A., Rozalska B., Bak-Romaniszyn L., Czkwianianc E., Planeta-Malecka I., Rechcinski T., Rudnicka W., Chmiela M.
Polish Journal of Microbiology
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2006
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tom 55
|
nr 2
Considering the role of lectin-carbohydrate interactions between Helicobacter pylori bacteria and the host cells we addressed the question on how mannose binding lectin - MBL, present in human plasma, may influence the phagocytosis of H. pylori by peripheral blood granulocytes. For phagocytosis assay the granulocytes separated from peripheral blood of healthy H. pylori-seronegative donors were used. Phagocytosis was estimated by fluorescence assay using FITC-labelled H. pylori cells. The MBL level in the serum samples as well as MBL-binding to H. pylori bacteria were estimated by ELISA. In this study all H. pylori isolates bound recombinant mannose binding lectin-MBL as shown by ELISA. The ingestion of H. pylori bacteria in the medium with human serum depleted in natural MBL (nMBL) was more intensive than in the medium with complete serum containing nMBL. Moreover, the ingestion of H. pylori bacteria in the medium with complete serum was increased by an addition of anti-rMBL IgG. The results indicate that interaction of bacterial and host lectins may regulate the phagocytosis of H. pylori bacteria and in this way influence an outcome of the infection caused by these microbes.
4

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
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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.
5

Potential role of LPS in the outcome of Helicobacter pylori related diseases

68%
Grebowska A., Rechcinski T., Bak-Romaniszyn L., Czkwianianc E., Moran A., Druszczynska M., Kowalewicz-Kulbat M., Owczarek A., Dziuba M., Krzeminska-Pakula M., Planeta-Malecka I., Rudnicka W., Chmiela M.
Polish Journal of Microbiology
|
2006
|
tom 55
|
nr 1
In this study we asked a question whether H. pylori LPS with or without LewisXY (Le) determinants as well as LBP (lipopolysaccharide binding protein) and sCD14 molecules recognizing bacterial LPS may be involved in atherogenesis. Sera from 57 patients with coronary heart disease (CHD), 27 H. pylori infected dyspeptic patients-H.p.(+) and 49 healthy controls (HC) were tested for IgM and IgG to H. pylori LPS expressing LeX (LPS LeX) or LeXY (LPS LeXY) determinants and to a glycine acid extract (GE). Immune complexes (ICs) of Lewis antigens and specific IgM or IgG were also determined. The prevalence of anti-GE IgG and IgA was significantly higher in CHD as compared to HC and the same as in the H.p.(+) group. The highest levels of anti-GE IgG were detected only for CHD group. CHD patients showed upregulation of IgG to LPS LeX and LeXY. In contrast, an upregulation of IgM to such LPSs was found for healthy subjects. The levels of LeY-anti-LeY IgG ICs were higher in CHD patients than in healthy controls similarly to the levels of LBP. There was no difference in sCD14 concentration between CHD and HC groups. The results obtained in this study indicate that H. pylori infections may be the risk factors of atherosclerosis due to: 1) an enhanced humoral response to H. pylori surface antigens, 2) a host predisposition to respond to Lewis determinants present in H. pylori LPS by IgG, 3) increased levels of serum LBP.
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