Wyniki wyszukiwania - Biblioteka Nauki

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Bakterie w bioremediacji gleby

100%

Gonciarz W.

Edukacja Biologiczna i Środowiskowa

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2013

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nr 3

17-22

EN

Bioremediation is biological technology of removing chemical substances of different kinds from soils, bottom sediments, active sediments, water, and air. It utilizes capability of living microorganisms, which can catalyze, destruct or transform various types of pollutants, into less harmful forms. Unfortunately, many substances can act as a contamination introduced into the environment causing ecological imbalance or disappearance of diffe rent trophic levels of the food chain. Bioremediation uses natural ability of microorganisms to degrade hydrocarbons. The main objective of this process is the mineralization of toxic organic compounds, leading ultimately to the formation of non-toxic substances like CO2, H2O and biomass. Hydrocarbons, such as derivatives of petroleum, in metabolic transformation of microorganisms constitute their carbon and energy sources, and can act as an acceptor of electrons. However, the rate of utilization of above-mentioned substances by microorganisms depends largely on the chemical nature of substance being degraded, as well as environmental factors, which can stimulate or inhibit these processes.

PL

Bioremediacja to biologiczna technologia usuwania różnego rodzaju substancji chemicznych z gleb, osadów dennych, osadów czynnych, wód i powietrza za pomocą mikroorganizmów. Znajdujące się w tych mikroorganizmach enzymy katalizują reakcje prowadzące do destrukcji lub transformacji różnego rodzaju zanieczyszczeń w formy mniej szkodliwe. Skażenie może wywołać każda substancja wprowadzana do środowiska powodująca zachwianie równowagi ekologicznej lub zanikanie poszczególnych poziomów troficznych łańcucha pokarmowego. W bioremediacji wykorzystywane są naturalne zdolności mikroorganizmów do rozkładu węglowodorów. Głównym celem tego procesu jest mineralizacja toksycznych związków organicznych, prowadząca ostatecznie do powstania nietoksycznych substancji, takich jak: CO2, H2O i biomasa. Węglowodory, takie jak pochodne ropy naftowej, w przemianach metabolicznych drobno ustrojów stanowią ich źródło węgla lub energii albo pełnią rolę akceptora elektronów w łańcuchu oddechowym. Jednakże stopień wykorzystania tych substancji przez mikroorganizmy zależy w dużej mierze od rodzaju degradowanej substancji, a także czynników środowiskowych, które mogą stymulować lub hamować przebieg tego procesu.

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The microbiological, histological, immunological and molecular determinants of Helicobacter pylori infection in guinea pigs as a convenient animal model to study pathogenicity of these bacteria and the infection dependent immune response of the host

38%

Walencka M. , Gonciarz W. , Mnich E. , Gajewski A. , Stawerski P. , Knapik-Dabrowicz A. , Chmiela M.

Acta Biochimica Polonica

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2015

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tom 62

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nr 4

697-706

EN

Helicobacter pylori is an etiological agent of chronic gastritis, gastric and duodenal ulcers and gastric cancers. The use of an appropriate animal model for experimental studies on the pathogenesis of H. pylori infections is necessary due to the chronic character of such infections and difficulties in identifying their early stage in humans. The aim of this study was to develop a guinea pig model of H. pylori infection and identify its microbiological, histological, serological and molecular determinants. Guinea pigs were inoculated per os with H. pylori strains: CCUG 17874 or ATCC 700312, both producing vacuolating cytotoxin A (VacA) and cytotoxin associated gene A (CagA) protein, suspended in Brucella broth with fetal calf serum (FCS) and Skirrow supplement of antibiotics. To determine H. pylori colonization, 7 and 28 days after the challenge, a panel of diagnostic methods was used. It included culturing of microorganisms from the gastric tissue, histopathological analysis of gastric sections, stained by Mayer,s haematoxylin and eosin to assess inflammatory response, by Giemsa as well as Warthin-Starry silver staining to visualise Helicobacter-like organisms (HLO) and with anti-Ki-67 antigen to assess epithelial cell proliferation. H. pylori infection was also confirmed by polymerase chain reactions (PCR) for detection in gastric tissue of ureC and cagA genes and by serological assessment of H. pylori antigens in faeces. This study showed the usefulness of microbiological, histological, immunological and molecular methods for the detection of persistent H. pylori infections in guinea pigs, which could be an appropriate model for studying H. pylori pathogenesis and the related immune response against these microbes.

3

Immunoregulation of antigen presenting and secretory functions of monocytic cells by Helicobacter pylori antigens in relation to impairment of lymphocyte expansion

32%

Mnich E. , Gajewski A. , Rudnicka K. , Gonciarz W. , Stawerski P. , Hinc K. , Obuchowski M. , Chmiela M.

Acta Biochimica Polonica

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2015

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tom 62

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nr 4

641-650

EN

The role of Helicobacter pylori (H. pylori) antigens in driving a specific immune response against the bacteria causing gastroduodenal disorders is poorly understood. Using a guinea pig model mimicking the natural history of H. pylori infection, we evaluated the effectiveness of immature and mature macrophages in promoting the blastogenesis of splenocytes from H. pylori infected and uninfected animals, in response to H. pylori antigens: glycine acid extract (GE), cytotoxin associated gene A protein (CagA), urease A (UreA) and lipopolysaccharide (LPS). Lymphocyte expansion was assessed in 72 h cell cultures, containing: immature or mature macrophages derived from bone marrow monocytes, unstimulated or stimulated with H. pylori antigens for 2 h. The proliferation was expressed as a ratio of [3H]-thymidine incorporation into DNA of antigen-stimulated to unstimulated cells and the DNA damage was determined by DAPI cell staining. TGF-β and IFN-γ were assessed immunoenzymatically in cell culture supernatants. Lymphocytes of control and H. pylori-infected animals proliferated intensively in response to phytohaemagglutinin (PHA) and in co-cultures with immature or mature macrophages treated with CagA or UreA (significantly) and GE (slightly) exluding the cultures containing H. pylori or E. coli LPS. This lymphocyte growth inhibition was related to DNA damage of monocytic cells in response to H. pylori or E. coli LPS and secretion of regulatory TGF-β, but not proinflammatory IFN-γ. Impaired homeostasis of monocytic cell function related to DNA damage and TGF-β release, in response to H. pylori LPS may lead to the suppression of adaptive immune response against the bacteria and development of chronic infection.