Other affiliations: Lund University
Bio: Galina Novik is an academic researcher from National Academy of Sciences of Belarus. The author has contributed to research in topics: Pseudomonas & Thyroid peroxidase. The author has an hindex of 10, co-authored 37 publications receiving 534 citations. Previous affiliations of Galina Novik include Lund University.
TL;DR: Structures governing phage recognition of host cell and mechanisms of phage adsorption and penetration into microbial cell are reviewed.
Abstract: Bacteriophages are an attractive tool for application in the therapy of bacterial infections, for biological control of bacterial contamination of foodstuffs in the alimentary industry, in plant protection, for control of water-borne pathogens, and control of environmental microflora. This review is mainly focused on structures governing phage recognition of host cell and mechanisms of phage adsorption and penetration into microbial cell.
TL;DR: In this paper, a green technique to obtain stable silver nanoparticles using reducing and stabilizing capacity of natural polysaccharide pectin was proposed, and the relationship between physico-chemical characteristics of formed Pectin-capped Silver nanoparticles and type of used pectins, as well as synthesis conditions was determined.
Abstract: The development of environmentally friendly, non-toxic and cheap technology for synthesis of silver nanoparticles with desired properties is currently under intensive investigation because such materials show huge potential for numerous biomedical applications. In this paper, we propose the ‘green’ technique to obtain stable silver nanoparticles using reducing and stabilizing capacity of natural polysaccharide pectin. The relationship between physico-chemical characteristics of formed pectin-capped silver nanoparticles and type of used pectin, as well as synthesis conditions, has been determined. Pectin-Ag nanocomposites were produced via reduction of silver nitrate by pectin in alkaline medium at room temperature. The synthesized nanoparticles were characterized by ultraviolet-visible and Fourier-transform infrared spectroscopy, X-ray diffraction analysis, transmission electron microscopy and dynamic light scattering. It has been established that pectin-capped silver nanoparticles have a spherical shape with a mean diameter from 8 to 28 nm, a negative charge and an absorption maximum in the range from 401 to 412 nm, depending on the type of pectin constituent. Antibacterial activity of the free pectins and their nanocomposites with Ag0 was evaluated by diffusion and suspension methods against both gram-positive (Bacillus pumilus, Bacillus subtilis) and gram-negative (Escherichia coli) bacteria. The size and composition-dependent antibacterial activity of ‘green’ synthesized silver nanoparticles has been demonstrated. It has been shown that among the pectin varieties only amidated one displayed antibacterial action on Bacillus strains: the minimum inhibitory concentration (MIC) was 3.4–7.1 mg mL−1. It has been found that antibacterial activity of pectin-capped silver nanoparticles depended on the type of introduced pectin and its ratio. The synthesized nanoparticles exhibited significant antimicrobial activity toward gram-negative bacteria Escherichia coli (MIC 0.18-0.39 mM) as compared with gram-positive Bacillus bacteria (MIC 0.39–1.55 mM).
TL;DR: The data are arguments in favour of the assumption of the possible role of PM of the genera Bifidobacterium and Lactobacillus in triggering ATD by the mechanism of molecular mimicry.
Abstract: During recent years, researchers have been focusing on the concept of an infectious etiology of autoimmune diseases. The most discussed theory is molecular mimicry, i.e. the emergence of autoreactive clones of T- and B-lymphocytes as a result of cross-immune response to homologous bacterial or viral antigen. Information on the role of probiotic microorganisms (PM) in the molecular mechanisms of autoimmune thyroid diseases (ATD) is limited. Using proteins and immunogenic peptides databanks and relevant computer programs, the homology between the amino acid sequences of thyroid peroxidase (TPO) and thyroglobulin (Tg), which are potential B- and T-cell epitopes of these antigens, and proteins of bifidobacteria and lactobacilli was established. Moreover, we have found components of cells of Bifidobacterium bifidum 791, Bifidobacterium adolescentis 94 BIM, Bifidobacterium longum B379M and Lactobacillus plantarum B-01 that selectively bind human antibodies to TPO (anti-TPO) and antibodies to Tg (anti-Tg) and compete with natural antigens for the binding of anti-TPO and anti-Tg in ELISA. Additionally, a three-fold difference was observed between the probability of detecting antibodies (Abs) to the antigens of L. plantarum B-01 and B. bifidum 791 in serum samples containing and those not containing anti-TPO. On the whole, our data are arguments in favour of the assumption of the possible role of PM of the genera Bifidobacterium and Lactobacillus in triggering ATD by the mechanism of molecular mimicry. The data obtained in silico and in vitro should be proven by use of animal models and clinical studies for extrapolations to the whole body. Possible antigenic properties of components/proteins of bifidobacteria and lactobacilli, selectively binding anti-TPO and anti-Tg should be taken into consideration. Natural human Abs to these bacterial components are probably able to cross-react with the TPO and Tg in the ELISA for detection of anti-TPO and anti-Tg, which are serologic markers of ATD. It can lead to unspecific false positive results and, hence, to an incorrect diagnosis.
TL;DR: The article is mainly devoted to such representatives of gut microbiota as lactic acid bacteria and bifidobacteria, with minor accent on less frequently used or new probiotic microorganisms.
Abstract: The article is mainly devoted to such representatives of gut microbiota as lactic acid bacteria and bifidobacteria, with minor accent on less frequently used or new probiotic microorganisms. Positive effects in treatment and prevention of diseases by different microbial groups, their metabolites and mechanisms of action, management and market of probiotic products are considered.
16 Jul 2015
TL;DR: Ability to degrade and produce a whole spectrum of compounds makes these species perspec‐ tive in industrial applications and opens up new frontiers for further use of Pseudomonas in various areas.
Abstract: Pseudomonas is a widespread bacterial genus embracing a vast number of species. Various genosystematic methods are used to identify Pseudomonas and differentiate these bacteria from species of the same genus and species of other genera. Ability to degrade and produce a whole spectrum of compounds makes these species perspec‐ tive in industrial applications. It also makes possible to use various media, including wastes, for cultivation of Pseudomonas. Pseudomonads may be applied in bioreme‐ diation, production of polymers and low-molecular-weight compounds, biocontrol. Recent studies open up new frontiers for further use of Pseudomonas in various areas.
TL;DR: It is shown that the type VI secretion system of Pseudomonas aeruginosa breaches this barrier to deliver two effector proteins, Tse1 and Tse3, to the periplasm of recipient cells, indicating a mechanism for export whereby effectors do not access donor cellperiplasm in transit.
Abstract: Peptidoglycan is the major structural constituent of the bacterial cell wall, forming a meshwork outside the cytoplasmic membrane that maintains cell shape and prevents lysis. In Gram-negative bacteria, peptidoglycan is located in the periplasm, where it is protected from exogenous lytic enzymes by the outer membrane. Here we show that the type VI secretion system of Pseudomonas aeruginosa breaches this barrier to deliver two effector proteins, Tse1 and Tse3, to the periplasm of recipient cells. In this compartment, the effectors hydrolyse peptidoglycan, thereby providing a fitness advantage for P. aeruginosa cells in competition with other bacteria. To protect itself from lysis by Tse1 and Tse3, P. aeruginosa uses specific periplasmically localized immunity proteins. The requirement for these immunity proteins depends on intercellular self-intoxication through an active type VI secretion system, indicating a mechanism for export whereby effectors do not access donor cell periplasm in transit.
TL;DR: The various tactics that are used by phages to overcome bacterial resistance mechanisms, including adsorption inhibition, restriction–modification, CRISPR–Cas (clustered regularly interspaced short palindromic repeats–CRISPR-associated proteins) systems and abortive infection are described.
Abstract: Bacteria and their viral predators (bacteriophages) are locked in a constant battle. In order to proliferate in phage-rich environments, bacteria have an impressive arsenal of defence mechanisms, and in response, phages have evolved counter-strategies to evade these antiviral systems. In this Review, we describe the various tactics that are used by phages to overcome bacterial resistance mechanisms, including adsorption inhibition, restriction-modification, CRISPR-Cas (clustered regularly interspaced short palindromic repeats-CRISPR-associated proteins) systems and abortive infection. Furthermore, we consider how these observations have enhanced our knowledge of phage biology, evolution and phage-host interactions.
TL;DR: Current research on the use of phages and their lytic proteins, specifically against multidrug-resistant bacterial infections, suggests phage therapy has the potential to be used as either an alternative or a supplement to antibiotic treatments.
Abstract: The practice of phage therapy, which uses bacterial viruses (phages) to treat bacterial infections, has been around for almost a century. The universal decline in the effectiveness of antibiotics has generated renewed interest in revisiting this practice. Conventionally, phage therapy relies on the use of naturally-occurring phages to infect and lyse bacteria at the site of infection. Biotechnological advances have further expanded the repertoire of potential phage therapeutics to include novel strategies using bioengineered phages and purified phage lytic proteins. Current research on the use of phages and their lytic proteins, specifically against multidrug-resistant bacterial infections, suggests phage therapy has the potential to be used as either an alternative or a supplement to antibiotic treatments. Antibacterial therapies, whether phage- or antibiotic-based, each have relative advantages and disadvantages; accordingly, many considerations must be taken into account when designing novel therapeutic approaches for preventing and treating bacterial infections. Although much is still unknown about the interactions between phage, bacteria, and human host, the time to take phage therapy seriously seems to be rapidly approaching.
TL;DR: An open-access resource, the Phage Receptor Database (PhReD), is established to serve as a repository for information on known and newly identified phage receptors involved in recognition and adsorption and their interactions during attachment.
Abstract: The adsorption of bacteriophages (phages) onto host cells is, in all but a few rare cases, a sine qua non condition for the onset of the infection process. Understanding the mechanisms involved and the factors affecting it is, thus, crucial for the investigation of host-phage interactions. This review provides a survey of the phage host receptors involved in recognition and adsorption and their interactions during attachment. Comprehension of the whole infection process, starting with the adsorption step, can enable and accelerate our understanding of phage ecology and the development of phage-based technologies. To assist in this effort, we have established an open-access resource--the Phage Receptor Database (PhReD)--to serve as a repository for information on known and newly identified phage receptors.
TL;DR: Studies on the role of autoreactive T-cells that are generated secondary to molecular mimicry, the diversity of the T-cell receptor repertoires of auto-reactiveT-cells, the roles of exposure to cryptic antigens, the generation of autoimmune B-cell responses, the interaction of microbiota and chemical adjuvants with the host immune systems all provide clues in advancing the understanding of the molecular mechanisms involved in the evolving concept of Molecular mimicry.
Abstract: Molecular mimicry is one of the leading mechanisms by which infectious or chemical agents may induce autoimmunity. It occurs when similarities between foreign and self-peptides favor an activation of autoreactive T or B cells by a foreign-derived antigen in a susceptible individual. However, molecular mimicry is unlikely to be the only underlying mechanism for autoimmune responses; other factors such as breach in central tolerance, non-specific bystander activation, or persistent antigenic stimuli (amongst others) may also contribute to the development of autoimmune diseases. Host genetics, exposure to microbiota and environmental chemicals are additional links to our understanding of molecular mimicry. Our current knowledge of the detailed mechanisms of molecular mimicry is limited by the issues of prolonged periods of latency before the appearance of disease, the lack of enough statistical power in epidemiological studies, the limitations of the potential role of genetics in human studies, the relevance of inbred murine models to the diverse human population and especially the limited technology to systematically dissect the human T-cell repertoire and B-cell responses. Nevertheless, studies on the role of autoreactive T-cells that are generated secondary to molecular mimicry, the diversity of the T-cell receptor repertoires of auto-reactive T-cells, the role of exposure to cryptic antigens, the generation of autoimmune B-cell responses, the interaction of microbiota and chemical adjuvants with the host immune systems all provide clues in advancing our understanding of the molecular mechanisms involved in the evolving concept of molecular mimicry and also may potentially aid in the prevention and treatment of autoimmune diseases.