Nihon saikingaku zasshi. Japanese journal of bacteriology最新文献

Heterocyclic triazines and their derivatives have excellent biological activity and have been used as herbicides and anticancer drugs. A large number of derivatives were synthesized and their biological activity was investigated. Some bacteria synthesize the triazine derivatives such as Nostocine A, Toxoflavin, and Fluviol from GTP using enzymes similar to those in the synthesis pathway of Riboflavin (vitamin B2). These triazine derivatives show antibiotic activity. In particular, research on Toxoflavin has progressed as a toxin produced by bacteria that cause seedling rot and rice grain blight in rice. It has recently been revealed that Fluviol, which is produced by bacteria, acts to suppress the growth of pathogenic bacteria. This review will focus on triazine derivatives produced by bacteria.

Proteins in the cells are born (synthesized), work, and die (decomposed). In the life of a protein, its birth is obviously important, but how it dies is equally important in living organisms. Proteases secreted into the outside of cells are used to decompose the external proteins and the degradation products are taken as the nutrients. On the other hand, there are also proteases that decompose unnecessary or harmful proteins which are generated in the cells. In eukaryotes, a large enzyme complex called the proteasome is primarily responsible for degradation of such proteins. Bacteria, which are prokaryotes, have a similar system as the proteasome. We would like to explain the bacterial degradation system of proteins or the death of proteins, which is performed by ATP-dependent protease Clp, with a particular focus on the ClpXP complex, and with an aspect as a target for antibiotics against bacteria.

Enterohemorrhagic Escherichia coli (EHEC) is an important pathogen since more than 3,000 cases have been reported annually in Japan. With the advent of next-generation sequencing, it has become feasible to analyze numerous strains using whole-genome sequence (WGS) analysis, making its application to surveillance a realistic possibility. In this paper, we introduce the following research outcomes achieved by our group utilizing WGS analysis of EHEC: 1) development of a WGS analysis pipeline to enhance the accuracy of the surveillance, 2) investigation of the dynamics of mobile elements such as plasmids and phages, and 3) analysis of the phylogeny and pathogenicity of newly identified highly pathogenic EHEC strains.

To combat drug-resistant bacteria, it is essential to develop new antimicrobial agents with novel mechanisms of action that demonstrate therapeutic efficacy. Lysocin E, discovered by our group, is a novel antibiotic with a unique mechanism of action that targets menaquinone. Compared to other antibiotics, lysocin E exhibits extremely potent bactericidal activity in a very short time. In addition, unlike other antibiotics, the antimicrobial activity of lysocin E is enhanced by adding serum, which triggers a distinct adjuvant effect of host factors, thereby demonstrating its exceptional therapeutic efficacy. It has been suggested that lysocin E is effective against intractable Staphylococcus aureus infections, and pre-clinical studies are ongoing. Lysocin E has the potential to become a next-generation therapeutic agent that is distinct from conventional antibacterial drugs.

Rhodococcus equi is a facultative intracellular gram-positive coccobacillus which is a well-known cause of foal pneumonia and/or enteritis in equine veterinary medicine. More than 300 cases of R. equi infection have been reported since the first description of human disease in 1968. Most patients who become infected with R equi are immunocompromised, such as those infected with human immunodeficiency virus (HIV), recipients of organ transplantation, and patients receiving cancer treatment. However, there are increasing reports of the immunocompetent hosts. The pathogenicity of R. equi has been attributed to the presence of plasmid-encoded virulence-associated proteins (Vap). To date, three host-associated virulence plasmid types of R. equi have been identified as follows: the circular pVAPA and pVAPB, related, respectively, to equine and porcine isolates in 1991 and 1995, and a recently described linear pVAPN plasmid associated with bovine and caprine strains in 2015. More recently, these three plasmid types have been re-found in the human isolates which were isolated during 1980s to 1990s. Not only horses, but also pigs, goats, cattle and their environment should be considered as a potential source of R. equi for humans. In this review, we shed light on the current understanding of R. equi as an emerging zoonotic pathogen.

Horizontal gene transfer through transconjugation and natural transformation plays a major role in the spread of antimicrobial resistance. Although the phenomenon of genetic element transmission has long been known, the rapid increase in the number of antimicrobial resistant bacteria in recent years and the accompanying accumulation of genomic information have revealed that horizontal gene transfer contributes to genome plasticity in various ways. The author reported the molecular mechanism of the antimicrobial activity of the accessory factor bacteriocin encoded by the junctional transfer plasmid of Enterococcus faecalis, a representative Gram-positive opportunistic pathogen that is concerned as highly antimicrobial resistant, and found diversity in the selfimmune system based on epidemiological studies. In addition, the author established a technique to visualize and quantify genomic recombination by natural transformation in Streptococcus pneumoniae which is also one of the most concerns for antimicrobial resistance and vaccine escape, at single cells level resolution in real time. Focuses on outcome from these research, this paper introduces the molecular mechanisms that promote horizontal gene transmission and the prospects for their technological application.

Urinary tract infections (UTIs) are one of the most common infections. Uropathogenic Escherichia coli (UPEC) is the most common causative organism. Once UPEC enters the urinary tract, it infects the bladder and then ascends the urinary tract to the kidneys, where it causes pyelonephritis, a more severe form of the disease. While various virulence factors, including adhesions and cytotoxic factors to bladder epithelial cells, have been identified and their functions have been analyzed, the question remains, "How can UPEC, which is harmless in the intestinal tract, be induced to become pathogenic in the urinary tract?" and "How does UPEC ascend the urinary tract and infect the kidneys?" On the other hand, UPEC invades host cells and forms biofilm-like microcolonies that are resistant to various antimicrobial agents. We are working to solve this problem by identifying the factors responsible for the virulence of UPEC and the establishment of infection of the kidney, as well as the factors involved in microcolony formation and elucidating their functions. Here I outline the virulence expression of UPEC from bladder to kidney infection and the mechanism of UTI refractoriness, focusing on our studies.