Biomedical subjects
Publications and source records attributed to A Górski.
We describe bacteriophage therapy in the case of a healthcare worker whose gastrointestinal tract was colonized by methicillin-resistant Staphylococcus aureus (MRSA) with subsequent urinary tract infection caused by the same pathogen. Oral treatment with anti-MRSA phages resulted in eradication of the carrier status.
Mammals have become "an environment" for enterobacterial phage life cycles. Therefore it could be expected that bacteriophages adapt to them. This adaptation must comprise bacteriophage proteins. Gp Hoc seems to have significance neither for phage particle structure nor for phage antibacterial activity. It is evidently not necessary for the "typical" antibacterial actions of bacteriophages. But the rules of evolution make it improbable that gp Hoc really has no function, and non-essential genes of T4-type phages are probably important for phages' adaptation to their particular lifestyle. More interesting is the eukaryotic origin of gp Hoc: a resemblance to immunoglobulin-like proteins that reflects their evolutionary relation. Substantial differences in biological activity between T4 and a mutant that lacks gp Hoc were observed in a mammalian system. Hoc protein seems to be one of the molecules predicted to interact with mammalian organisms and/or modulate these interactions.
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Although there is much evidence supporting a prion contribution in the pathogenesis of transmissible spongiform encephalopathies, a novel point of view as to the induction of the diseases can be proposed. It is hypothesized that neurodegenerative diseases, such as scrapie in sheep and goats and bovine spongiform encephalopathy in cattle (BSE), originate from the consumption of glycated proteins contained in their feed. These components are obtained during a high-temperature glycation process.
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Beta2-microglobulin (beta2M) is the light chain of the class I HLA molecule. The serum level of beta2M is elevated in various diseases including lymphoma, inflammation, viral infections and chronic renal dysfunction. The present study addressed the possible influence of beta2M on T lymphocyte activation in vitro. Peripheral blood mononuclear cells from a group of 17 healthy subjects were examined. Stimulation with OKT3 and fibronectin in combination with 30 mg beta2M/dl resulted in a two-fold increase of cell proliferation. A similar effect was observed when OKT3 and collagen I were applied as well as when OKT3 and collagen IV were used as costimulation to T cells. The CD69 expression, measured by flow cytometry was significantly enhanced above the control level (1.52 +/- 1.03% vs 33.21 +/- 20.26%, p<0.01, control group and 30 mg beta2M/dl, respectively). Together, these observations suggest that beta2M may play a role in modulating lymphocyte proliferation, possibly through modification of the CD69 molecule.
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The influence of metronidazole on the level of expression of adhesion molecules ICAM-1, VCAM-1 and E-selectin on the surface of vascular endothelial cells activated with B. fragilis endotoxins and enterotoxin was examined. Three enterotoxigenic (ETBF) strains and one nonenterotoxigenic (NTBF) strain were used for lipopolysaccharide extraction. Enterotoxin was prepared from the culture supernatant of the reference B. fragilis ATCC 43858 strain. Expression of adhesion molecules on vascular endothelial cells (HMEC-1 cell line) was determined after their stimulation with bacterial compounds at the concentration of 10 micrograms/ml in the presence of metronidazole at the concentration of 4 micrograms/ml. Endothelial cells were activated for 4 hours (E-selectin expression) and for 24 hours (ICAM-1 and VCAM-1 expression). Adhesion molecules were detected in immunoenzymatic test (ELISA) with mouse, monoclonal antibodies against human ICAM-1, VCAM-1 and E-selectin. The results of experiments suggest, that metronidazole enhances the expression of examined adhesion molecules on endothelial cells. This antimicrobial agent causes some changes in the expression of endothelial ICAM-1, VCAM-1 and E-selectin stimulated by B. fragilis endotoxins and enterotoxin.
The influence of clindamycin on expression of B. fragilis endotoxins (LPS) and enterotoxin stimulated cell adhesion molecules: ICAM-1, VCAM-1 and E-selectin on HMEC-1 (human microvascular endothelial cell line) was tested. Lipopolysaccharides from four Bacteroides fragilis strains: one nonenterotoxigenic (NTBF) and three enterotoxigenic (ETBF) were extracted by hot phenol-water method and purified. B. fragilis enterotoxin was prepared according to the method described by van Tassel et al. (1992). All bacterial preparations were used for stimulation at concentration 10 micrograms/ml. Clindamycin was used in concentration of 2 micrograms/ml. The influence of antimicrobial agent on the endotoxins and enterotoxin stimulation and expression of adhesion molecules was tested by ELISA, using monoclonal mouse anti-human antibodies (Genzyme, USA). Peroxidase-conjugated rabbit anti-mouse immunoglobulins (DAKO A/S Denmark) and OPD (Sigma USA) were used. The coloured reaction product was measured by reading the absorbance at 492 nm in SPECTRA II reader (SLT, Austria). It was observed that clindamycin influenced the expression of cell adhesion molecules on resting cell line. HMEC-1 cells stimulated with Bacteroides fragilis LPS preparations have suppressive effect on ICAM-1 expression. ICAM-1 expression was augmented when stimulated with Tox 1 and Tox 2 preparations. Clindamycin augmented the VCAM-1 expression in tests with all bacterial preparations. All used bacterial preparations of Bacteroides fragilis LPS and enterotoxin enhanced the expression of E-selectin with exception of LPS of NTBF strain.
The aim of presented study was to estimates the number of human granulocytes and T lymphocytes adhering to 1 mm2 of vascular endothelial cell culture stimulated by Bacteroides fragilis endotoxins (LPS) and enterotoxin (BFT). HMEC-1 cells were activated with bacterial preparations at the concentration of 10 (micrograms/ml for 4 and 24 hours. Granulocytes and T lymphocytes were isolated from peripheral blood of healthy blood donors. The adhesion tests of granulocytes and adhesion tests of resting and activated with PMA (at the concentration of 10 ng/ml) T lymphocytes to the non-stimulated and stimulated by B. fragilis compounds (LPS and BFT) vascular endothelium were performed. The number of viable leukocytes, which adhered to the endothelium, was determined using inverted microscope (magnification 200x). The results were presented as the number of viable cells adhering to 1 mm2 of the endothelial cell culture. The results of experiments indicate that granulocytes and T lymphocytes (resting and after activation with PMA even in greater number) adhere to the endothelial cells stimulated by B. fragilis endotoxins and enterotoxin. B. fragilis toxins are weaker stimulants of human leukocyte adhesion to the HMEC-1 cells than E. coli O55:B5 LPS. B. fragilis LPS and BFT preparations stimulate endothelial cells to the adhesion of granulocytes in similar manner, whereas the activation of vascular endothelium to the adhesion of T lymphocytes is differentiated.
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Endometriosis is characterised by the presence of abnormally located tissue resembling the endometrium with glands and stroma. The abnormal endometrium of women affected by endometriosis could be able to protect itself from harmful effects of immune cells by expressing specific antigens, by harbouring a different population and by synthesizing and secreting immunosuppressive factors. This disturbance may be regulated by factors in peritoneal fluid which is a specific microenvironment.
beta 1 integrins, receptors responsible for the binding of extracellular matrix proteins, mediate activation, adhesion, migration and differentiation in different tissue compartments. It has been recently demonstrated that integrins are distributed on sperm surface and on T cells, as well. The aim of this study was to establish influence of antisperm antibodies on T cell adhesion to extracellular matrix proteins in women with a history of unexplained infertility.