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1

Isotypic analysis of anti-H.pylori antibodies in sera from children after anti-H.pylori treatment

100%
Czkwianianc E., Chmiela M., Bak-Romaniszyn L., Rudnicka W., Planeta-Malecka I.
Journal of Physiology and Pharmacology. Supplement
|
1997
|
tom 48
|
nr 1
2

Gastric and duodenal mucosa in children with duodenal ulcer before and after eradication of Helicobacter pylori

100%
Bak-Romaniszyn L., Planeta-Malecka I., Kulig A., Czkwianianc E., Suski S.
Journal of Physiology and Pharmacology. Supplement
|
1997
|
tom 48
|
nr 1
3
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Prevalence of Helicobacter pylori in children dependently on age and living conditions

100%
Czkwianianc E., Bak-Romaniszyn L., Malecka-Panas E., Suski S., Woch G.
Journal of Physiology and Pharmacology
|
1996
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tom 47
|
nr 1
4

Immune response to Helicobacter pylori in gastritis and duodenal ulcer in children

100%
Bak-Romaniszyn L., Zeman K., Czkwianianc E., Malecka-Panas E., Fornalczyk E.
Journal of Physiology and Pharmacology. Supplement
|
1997
|
tom 48
|
nr 1
5
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Changes in smoking prevalence and exposure to environmental tobacco smoke among adults in Łódź, Poland

86%
Fronczak A., Polanska K., Dziankowska-Zaborszczyk E., Bak-Romaniszyn L., Korytkowski P., Wojtyla A., Kaleta D.
Annals of Agricultural and Environmental Medicine
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2012
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tom 19
|
nr 4
6

Serological assessment H.pylori infection in children and adults with chronic gastritis and gastroduodenitis

86%
Czkwianianc E., Chmiela M., Lawnik M., Rechcinski T., Bak-Romaniszyn L., Planeta-Malecka I., Rudnicka W.
Journal of Physiology and Pharmacology. Supplement
|
1997
|
tom 48
|
nr 1
7

Estimation of IL-1beta and IL-8 in gastric juice and blood serum in children with Helicobacter pylori

86%
Bak-Romaniszyn L., Planeta-Malecka I., Czkwianianc E., Zeman K., Pokoca L., Kulig A.
Journal of Physiology and Pharmacology. Supplement
|
2001
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tom 52
|
nr 2
8

Pepsynogen I and gastrin level in children with Helicobacter pylori [Hp]

86%
Czkwianianc E., Planeta-Malecka I., Bak-Romaniszyn L., Malkowski B., Jurowska M., Maziarz Z., Kulig A.
Journal of Physiology and Pharmacology. Supplement
|
2001
|
tom 52
|
nr 2
9
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Helicobacter pylori infection in the etiopathogenesis of duodenal ulcer in children

72%
Bak-Romaniszyn L., Malecka-Panas E., Zeman K., Czkwianianc E., Kozlowski W., Kulig A., Kaluzynski A., Suski S.
Journal of Physiology and Pharmacology
|
1996
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tom 47
|
nr 1
10

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

72%
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.
11

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

72%
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
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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.
12

Serological differentiation of Helicobacter pylori CagA[plus] and CagA[minus] infections

72%
Chmiela M., Wisniewska M., Bak-Romaniszyn L., Rechcinski T., Planeta-Malecka I., Bielanski W., Konturek S. J., Plonka M., Klink M., Rudnicka W.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
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tom 51
|
nr 2
13

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

59%
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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