All posts by Postępy Mikrobiologii

Human Microbiome Project – mikroflora jelit oraz jej wpływ na fizjologię i zdrowie człowieka

Human Microbiome Project – influence of gut microbiota on human physiology and health
J. Olszewska, E. K. Jagusztyn-Krynicka

1. Wstęp. 2. HMP – ogólna charakterystyka. 3. Mikroflora jelit. 3.1. Różnorodność taksonomiczna mikroflory jelit człowieka. 3.2. „Core microbiome” jelit. 3.3. Zmiany mikroflory jelit w zależności od wieku. 3.4. Wpływ diety i genotypu gospodarza na różnorodność mikroflory jelit. 3.5. Wybrane funkcje mikroflory jelit. 3.6. Mikroflora jelit człowieka a choroby. 3.6.1. Nowotwory. 3.6.2. Otyłość. 4. Podsumowanie

Abstract: The HMP (Human Microbiome Project) is one of several international projects which use metagenomic analysis to study human health. The HMP is a logical conceptual and experimental extension of Human Genome Project. The first part of the review presents general characteristic of the project, its goals and implementation phases. The gastrointestinal tract microbiota is extremely dense and diverse. Microbiota genes encode many biochemical pathways that humans have not evolved. Gut microbiota composition is ins are associated with many diseases. This review summarizes the latest research concerning the association of gut microbial ecology with the mechanisms by which microbes in the gut may mediate host physiology and metabolism in the context of obesity and cancer.

1. Introduction. 2. HMP – general characteristic. 3. Gut microbiota. 3.1. Microbial diversity of the human gut microbiota. 3.2. Gastrointestinal tract core microbiome. 3.3. Intestinal microbiota composition over human life. 3.4. Influence of diet and human genotype on gut microbiota 3.5. Selected activities of gut microbiota 3.6. Gut microbiota and diseases. 3.6.1. Cancer. 3.6.2. Obesity. 4. Summary

Rola mikroflory jelit w indukcji choroby Leśniewskiego-Crohna w świetle programu badań Human Microbiome Project

Role of microbiota in Crohn’s disease induction in the light of studies of Human Microbiome Project
A. Franczuk, E. K. Jagusztyn-Krynicka

1. Wstęp. 2. Podłoże genetyczne i immunologiczne CD. 2.1. Podłoże genetyczne choroby Leśniowskiego-Crohna. 2.2. Defensyny. 2.3. Nabłonkowa bariera jelitowa. 3. Rola mikroflory jelit w indukcji CD. 3.1. Zmiany dysbiotyczne. 3.2. Organizacja przestrzenna mikroorganizmów flory jelit. 4. Przyszłość metagenomiki w badaniu CD. 5. Podsumowanie

Abstract: Crohn’s disease (CD) is an inflammatory disorder which develops as a result of dysregulated interactions between gut microbiota and immune system. Because bacterial involvement in this illness is certain and classic methods of growing microorganisms are insufficient to clarify their impact on disease induction, metagenomics, as a culture-independent technique, provides revolutionary approach. This method become pivotal tool for a large project aiming at describing whole human microbiota – Human Microbiome Project (HPM). Studies on pathologically changed gut microbiota of CD patients involving metagenomic strategy provide profound analysis of intestinal microbial structure as well microbial localization. Ee review article also presents various aspects of the immune system functioning – such as genetic predispositions, dysregulated defensin secretion, poor epithelial barrier integrity, which contribute to improper immunological answer and promotion of inflammation.

1. Introduction. 2. Genetic and immunological basis. 2.1. Genetic basis of CD. 2.2. Defensins. 2.3. Gut epithelial barrier. 3. Role of microbiota in CD induction. 3.1. Dysbiotic changes. 3.2. Spatial organization of gut microorganisms. 4. Future of metagenomics in studies on CD. 5. Summary

Dwuskładnikowe systemy regulacyjne ziarenkowców Gram-dodatnich i ich rola w tworzeniu biofilmu

The role of two-component regulatory systems of Gram-positive cocci in biofilm formation
A. Nowak, S. Tyski

1. Wstęp. 2. Budowa, sposób działania i autoregulacja dwuskładnikowych systemów regulacyjnych (TCS). 3. TCS a biofilm. 3.1. Biofilm paciorkowców. 3.1.1. System VicRK S. mutans. 3.1.2. System ComDE S. mutans. 3.1.3. System HK11/RR11 (LiaSR) S. mutans. 3.1.4. System CiaRH S. mutans. 3.1.5. System CovRS (CsrRS) paciorkowców grup A, B, C. 3.1.6. System BfrAB S. gordonii. 3.2. Biofilm gronkowców. 3.2.1. System ArlRS S. aureus. 3.2.2. System GraRS S. aureus. 3.2.3. System WalKR S. aureus. 3.2.4. System LytSR S. aureus. 3.2.5. System SaeRS S. aureus oraz S. epidermidis. 3.3. Biofilm enterokoków. 3.3.1. System FsrABC E. faecalis. 3.3.2. System EtaSR E. faecalis. 4. Podsumowanie

Abstract: Two-component systems (TCS) are common in bacterial cells and play an important role in response to various signals coming from environment. The simplest TCS consists of two elements: a membrane sensor protein, which receives signals and the other – a regulatory protein that modulates target gene expression in response to the stimulus. The recent studies have shown that biofilm formation is dependent on many genetic factors, including the two-component regulatory systems. The bacterial cells living in biofilm communities are very vital and resistant to many antibiotics and antimicrobial agents. Therefore, in-depth knowledge of TCS involved in biofilm formation seems to be necessary to combat the growing resistance of bacteria.
1. Introduction. 2. Structure, organization and autoregulation of two-component regulatory systems. 3. TCS and the biofilm. 3.1. Streptococcal biofilm. 3.1.1. The VicRK system of S. mutans. 3.1.2. The ComDE system of S. mutans. 3.1.3. The HK11/RR11 (LiaSR) system of S. mutans. 3.1.4. The CiaRH system of S. mutans. 3.1.5. The CovRS (CsrRS) system of grup A, B, C streptococci. 3.1.6. The BfrAB system of S. gordonii. 3.2. Staphylococcal biofilm. 3.2.1. The ArlRS system of S. aureus. 3.2.2. The GraRS system of S. aureus. 3.2.3. The WalKR system of S. aureus. 3.2.4. The LytSR system of S. aureus. 3.2.5. The SaeRS system of S. aureus and S. epidermidis. 3. Enterococcal biofilm. 3.3.1. The FsrABC system of E. faecalis. 3.3.2. The EtaSR system of E. faecalis . 4. Summar

Wewnątrzkomórkowe bakterie względnie chorobotwórcze w zakażeniach górnych dróg oddechowych i ucha

Intracellular opportunistic bacteria in upper respiratory tract and ear infections
E. A. Trafny
1. Wprowadzenie. 2. Czy komórki nabłonkowe i limfoidalne migdałków stanowią rezerwuar patogenów wywołujących nawracające zakażenia górnych dróg oddechowych (GDO) i ucha? 3. Adhezyny umożliwiające przyleganie patogenów GDO do komórek gospodarza. 3.1. Adhezyny bakterii Gram-ujemnych. 3.2. Adhezyny ziarenkowców Gram-dodatnich. 3.3. Wpływ niskiej temperatury na ekspresję genów kodujących adhezyny u patogenów GDO. 4. Mechanizmy internalizacji patogenów do komórek gospodarza. 5. Sposoby przetrwania patogenów GDO wewnątrz komórek ssaków. 6. Wrażliwość wewnątrzkomórkowych patogenów GDO na antybiotyki i chemioterapeutyki.
Abstract: The pathogens commonly causing the upper respiratory tract infections: Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, nontypeable Haemophilus influenzae and Moraxella catarrhalis are able to exist within host cells in human upper respiratory tract. They may be found both in homogenates of the adenoids and tonsils and inside epithelial and monocyte/macrophage cells isolated from these tissues. The bacteria also invade epithelium of middle ear mucosa. They are alive and can multiply in the cytoplasm. Numerous adhesins are responsible for a tight attachment of bacterial cells to epithelial and endothelial cells as well as to lymphocytes. These adhesins mediate bacterial internalization by human cells. Some bacteria, e.g. S. aureus, are able to persist viable within host cell compartments for several days in high numbers. Bacterial persistence in the cellular interior allows evading immunological defences and bactericidal activity of antimicrobials, thereby creating an intercellular reservoir of pathogenic and/or opportunistic bacteria. Antibacterial agents, even when are applied in doses exceeding the MIC values, do not eradicate these bacteria from the intracellular compartment. This feature of intracellular bacteria resembles the characteristic attributes of biofilms, i.e. their increased tolerance to bactericidal antimicrobials.
1. Introduction. 2. Do epithelial and lymphoid cells constitute a reservoir of pathogens causing recurrent infections of upper respiratory tract (URT) and ear? 3. Adhesins that facilitate attachment of UTR pathogens to host cells. 3. Adhesins of Gram-negative bacteria. 3.2. Adhesins of Gram-positive coccal bacteria. 3.3. The effect of low temperature on the expression of the genes encoding adhesins of URT pathogens. 4. The internalization mechanisms of URT pathogens into host cells. 5. Bacterial strategies to persist within mammalian cells. 6. Susceptibility of the intracellular URT pathogens toward antibiotics.

Czynniki wirulencji Staphylococcus aureus zależne od bakteriofagów

Phage-related virulence factors of Staphylococcus aureus
W. M. Helbin, K. Polakowska, J. Międzobrodzki

1. Wprowadzenie. 2. Wpływ bakteriofagów na wirulencję gatunku Staphylococcus aureus. 3. Gronkowcowe wyspy patogenności SaPIs (staphylococcal pathogenicity islands). 4. Wpływ antybiotyków na odpowiedź SOS i indukcję bakteriofagów. 5. Podsumowanie

Abstract: Mobile genetic elements play fundamental role in the emergence of new pathogens and in the adaptation of all bacteria species to the enviromnent. It is believed that the horizontal gene transfer has a major impact on genome structure of Staphylococcus aureus which of both commensal and major pathogen of humans and warm-blooded animals. Bacteriophages via lysogenic conversion are source of the major staphylococcal virulence factors, contribute to strain diversity and enable rapid changes in host specificity. Bacteriophages have also close connection to other kind of mobile genetic elements, known as staphylococcal pathogenicity islands, SaPIs. SaPIs excision from chromosome and replication is possible only after infection of a particular phage and the islands are able to leave the host cell inside hijacked capsids. Horizontal transfer of SaPIs which occurs through a modified transduction may be responsible for spread of toxic-shock syndrome toxin TSST-1, and other superantigenes among S. aureus
strains, and possibly from S. aureus to other species. Recently it has been reported that β-lactam and fluorochinolone antibiotic in subinhibitory concentration promote SOS-mediated prophage induction, replication of SaPIs in its host cells and consequently the further spread of SaPIs, and lysogenic conversion genes in pathogenic bacteria. Further understanding of phage and phage-dependent mobile genetic elements can provide insight into staphylococcal virulence and help in the development of efficient treatment of S. aureus infections.
1. Introduction. 2. Effect of bacteriophages on the virulence of Staphylococcus aureus. 3. Staphylococcal pathogenicity islands SaPIs. 4. Antibiotic dependent SOS response and the induction of prophages. 5. Summary

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Najnowszy numer

2018, 57, 1

O Towarzystwie


Celem Polskiego Towarzystwa
Mikrobiologów jest propagowanie rozwoju nauk mikrobiologicznych

i popularyzowanie osiągnięć
mikrobiologii wśród członków Towarzystwa oraz szerokich kręgów społeczeństwa. Formami działalności jest organizowanie zjazdów, posiedzeń naukowych, kursów, wykładów
i odczytów oraz konkursów prac naukowych; wydawanie i popieranie wydawania czasopism naukowych, książek
i innych publikacji
z dziedziny mikrobiologii; opiniowanie o stanie i potrzebach mikrobiologii polskiej

i występowanie w jej sprawach wobec
władz państwowych; współpraca
z pokrewnymi stowarzyszeniami
w kraju i za granicą.