The oral cavity is inhabited by more than 600 bacterial species; these species compete for nutrients or coexist in order to survive along with the indigenous population. Extreme conditions are prevalent in the oral cavity, and these conditions are influenced by our immunity and variations in nutrition, temperature, and pH. Pathogens that cause dental caries or periodontal disease can survive in these extreme environments; these pathogens are virulent and can cause several diseases. Therefore, research on oral bacteriology is warranted to analyze the virulence factors of these bacteria as well as to ascertain environmental stress responses, interactions between bacteria and human immunity, comparisons of bacterial genomes, and oral microflora. In this review, we provide new data in the fields of bacteriology, immunology, and genomics and describe recent advances in the field of oral bacteriology.
{"title":"[Recent advances in the field of oral bacteriology].","authors":"Mikio Shoji, Toru Takeshita, Fumito Maruyama, Hiroaki Inaba, Kenichi Imai, Miki Kawada-Matsuo","doi":"10.3412/jsb.70.333","DOIUrl":"https://doi.org/10.3412/jsb.70.333","url":null,"abstract":"<p><p>The oral cavity is inhabited by more than 600 bacterial species; these species compete for nutrients or coexist in order to survive along with the indigenous population. Extreme conditions are prevalent in the oral cavity, and these conditions are influenced by our immunity and variations in nutrition, temperature, and pH. Pathogens that cause dental caries or periodontal disease can survive in these extreme environments; these pathogens are virulent and can cause several diseases. Therefore, research on oral bacteriology is warranted to analyze the virulence factors of these bacteria as well as to ascertain environmental stress responses, interactions between bacteria and human immunity, comparisons of bacterial genomes, and oral microflora. In this review, we provide new data in the fields of bacteriology, immunology, and genomics and describe recent advances in the field of oral bacteriology. </p>","PeriodicalId":19308,"journal":{"name":"Nihon saikingaku zasshi. Japanese journal of bacteriology","volume":"70 2","pages":"333-8"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3412/jsb.70.333","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33348653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nitric oxide (NO) and reactive oxygen species (ROS) produced during infection are involved critically in host defense mechanisms. It is quite important to physiologically regulate ROS, such as superoxide, and NO. These reactive species produced in excess may cause oxidative damage of biological molecules. An important cytoprotective and antimicrobial function of NO and ROS is mediated by induction of heme oxygenase (HO)-1. The signaling mechanism of this HO-1 induction has remained unclear, however. We discovered in 2007 a unique second messenger, 8-nitroguanosine 3',5'-cyclic monophosphate (8-nitro-cGMP), that mediates electrophilic signal transduction during oxidative stress and other cellular redox signaling in general. 8-Nitro-cGMP is formed via guanine nitration with NO and ROS, and in fact, NO-dependent 8-nitro-cGMP formation and HO-1 induction were identified in Salmonella-infected mice. HO-1 induction was regulated solely by 8-nitro-cGMP formed in cells, and more important, its potent anti-apoptotic function was evident in such a Salmonella infection. 8-Nitro-cGMP has a potent cytoprotective function, of which signaling appears to be mediated via protein sulfhydryls to generate a post-translational modification called protein S-guanylation. 8-Nitro-cGMP specifically S-guanylates Keap1, a negative regulator of transcription factor Nrf2, which in turn up-regulates transcription of HO-1. Our recent study revealed that the autophagy might be involved in the 8-nitro-cGMP-dependent antimicrobial effect. The 8-nitro-cGMP signaling was also found to be regulated by reactive sulfur species that have superior antioxidant activity and unique signaling function. This review will discuss a new paradigm of the host defense that operates via formation of a unique cell signaling molecule, 8-nitro-cGMP, during microbial infections.
{"title":"[Host defense and oxidative stress signaling in bacterial infection\u2029].","authors":"Takaaki Akaike","doi":"10.3412/jsb.70.339","DOIUrl":"https://doi.org/10.3412/jsb.70.339","url":null,"abstract":"<p><p>Nitric oxide (NO) and reactive oxygen species (ROS) produced during infection are involved critically in host defense mechanisms. It is quite important to physiologically regulate ROS, such as superoxide, and NO. These reactive species produced in excess may cause oxidative damage of biological molecules. An important cytoprotective and antimicrobial function of NO and ROS is mediated by induction of heme oxygenase (HO)-1. The signaling mechanism of this HO-1 induction has remained unclear, however. We discovered in 2007 a unique second messenger, 8-nitroguanosine 3',5'-cyclic monophosphate (8-nitro-cGMP), that mediates electrophilic signal transduction during oxidative stress and other cellular redox signaling in general. 8-Nitro-cGMP is formed via guanine nitration with NO and ROS, and in fact, NO-dependent 8-nitro-cGMP formation and HO-1 induction were identified in Salmonella-infected mice. HO-1 induction was regulated solely by 8-nitro-cGMP formed in cells, and more important, its potent anti-apoptotic function was evident in such a Salmonella infection. 8-Nitro-cGMP has a potent cytoprotective function, of which signaling appears to be mediated via protein sulfhydryls to generate a post-translational modification called protein S-guanylation. 8-Nitro-cGMP specifically S-guanylates Keap1, a negative regulator of transcription factor Nrf2, which in turn up-regulates transcription of HO-1. Our recent study revealed that the autophagy might be involved in the 8-nitro-cGMP-dependent antimicrobial effect. The 8-nitro-cGMP signaling was also found to be regulated by reactive sulfur species that have superior antioxidant activity and unique signaling function. This review will discuss a new paradigm of the host defense that operates via formation of a unique cell signaling molecule, 8-nitro-cGMP, during microbial infections. </p>","PeriodicalId":19308,"journal":{"name":"Nihon saikingaku zasshi. Japanese journal of bacteriology","volume":"70 3","pages":"339-49"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3412/jsb.70.339","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34124915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Proactive approaches to collect precise information are necessary to control infectious diseases in the whole world. A collaborative research for infectious diseases with institute or university of countries that infectious diseases occur is one of the good approaches. In this paper, we introduce collaborative researches on infectious diseases with Asian countries, such as Vietnam, Philippines, Thailand, and India.
{"title":"[Infectious diseases in Asia/International collaboration in bacterial infectious diseases].","authors":"Mitsutoshi Senoh, Masatomo Morita","doi":"10.3412/jsb.70.329","DOIUrl":"https://doi.org/10.3412/jsb.70.329","url":null,"abstract":"<p><p>Proactive approaches to collect precise information are necessary to control infectious diseases in the whole world. A collaborative research for infectious diseases with institute or university of countries that infectious diseases occur is one of the good approaches. In this paper, we introduce collaborative researches on infectious diseases with Asian countries, such as Vietnam, Philippines, Thailand, and India. </p>","PeriodicalId":19308,"journal":{"name":"Nihon saikingaku zasshi. Japanese journal of bacteriology","volume":"70 2","pages":"329-32"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3412/jsb.70.329","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33348652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mycoplasmas are smallest organisms capable of self-replication and cause various diseases in human. Especially, Mycoplasma pneumoniae is known as an etiological agent of pneumonia. From 2010 to 2012, epidemics of M. pneumoniae infections were reported worldwide (e.g., in France, Israel, and Japan). In the diseases caused by mycoplasmas, strong inflammatory responses induced by mycoplasmas have been thought to be important. However, mycoplasmas lack of cell wall and do not possess inflammation-inducing endotoxin such as lipopolysaccharide (LPS). We purified inflammation-inducing factors from pathogenic mycoplasmas and identified that they were lipoproteins. Lipoproteins derived from mycoplasmas induced inflammatory responses through Toll-like receptor (TLR) 2. In addition, we demonstrated that cytadherent property of M. pneumoniae played an important role in induction of inflammatory responses. Cytadherent property of M. pneumoniae induced inflammatory responses through TLR2 independent pathway. TLR4, inflammasomes, and autophagy were involved in this TLR2 independent induction of inflammatory responses.
{"title":"[Pathogenic factors of mycoplasma].","authors":"Takashi Shimizu","doi":"10.3412/jsb.70.369","DOIUrl":"https://doi.org/10.3412/jsb.70.369","url":null,"abstract":"Mycoplasmas are smallest organisms capable of self-replication and cause various diseases in human. Especially, Mycoplasma pneumoniae is known as an etiological agent of pneumonia. From 2010 to 2012, epidemics of M. pneumoniae infections were reported worldwide (e.g., in France, Israel, and Japan). In the diseases caused by mycoplasmas, strong inflammatory responses induced by mycoplasmas have been thought to be important. However, mycoplasmas lack of cell wall and do not possess inflammation-inducing endotoxin such as lipopolysaccharide (LPS). We purified inflammation-inducing factors from pathogenic mycoplasmas and identified that they were lipoproteins. Lipoproteins derived from mycoplasmas induced inflammatory responses through Toll-like receptor (TLR) 2. In addition, we demonstrated that cytadherent property of M. pneumoniae played an important role in induction of inflammatory responses. Cytadherent property of M. pneumoniae induced inflammatory responses through TLR2 independent pathway. TLR4, inflammasomes, and autophagy were involved in this TLR2 independent induction of inflammatory responses.","PeriodicalId":19308,"journal":{"name":"Nihon saikingaku zasshi. Japanese journal of bacteriology","volume":"376 1","pages":"369-74"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75126547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Bacteria have various way to move over solid surfaces, such as glass, agar, and host cell. These movements involve surface appendages including flagella, type IV pili and other "mysterious" nano-machineries. Gliding motility was a term used various surface movements by several mechanisms that have not been well understood in past few decades. However, development of visualization techniques allowed us to make much progress on their dynamics of machineries. It also provided us better understanding how bacteria move over surfaces and why bacteria move in natural environments. In this review, I will introduce recent studies on the gliding motility of Flavobacteium and Mycoplasma based on the detail observation of single cell and its motility machinery with micro-nano scales.
{"title":"[Mechanism of bacterial gliding motility].","authors":"Daisuke Nakane","doi":"10.3412/jsb.70.375","DOIUrl":"https://doi.org/10.3412/jsb.70.375","url":null,"abstract":"Bacteria have various way to move over solid surfaces, such as glass, agar, and host cell. These movements involve surface appendages including flagella, type IV pili and other \"mysterious\" nano-machineries. Gliding motility was a term used various surface movements by several mechanisms that have not been well understood in past few decades. However, development of visualization techniques allowed us to make much progress on their dynamics of machineries. It also provided us better understanding how bacteria move over surfaces and why bacteria move in natural environments. In this review, I will introduce recent studies on the gliding motility of Flavobacteium and Mycoplasma based on the detail observation of single cell and its motility machinery with micro-nano scales.","PeriodicalId":19308,"journal":{"name":"Nihon saikingaku zasshi. Japanese journal of bacteriology","volume":"61 1","pages":"375-82"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88797957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Staphylococcus aureus causes various diseases against humans, including skin infection, pneumonia, food poisoning, and meningitis. Methicillin-resistant S. aureus (MRSA) is resistant to a broad range of antibiotics, causing serious clinical problems. In this review, I summarize our studies to evaluate S. aureus virulence and identify novel virulence regulators. First, we utilized silkworms as an infection model of S. aureus and identified novel virulence factors of S. aureus. Some of the virulence factors interact with RNA in bacterial cells and regulate the expression of virulence factors. Second, we found that S. aureus cells spread on soft agar plates and form a giant colony. We call this phenomenon colony-spreading. High virulence community-acquired MRSA exhibits higher colony-spreading activity than hospital-associated MRSA. The difference in colony spreading is attributed to a specific gene in the mobile genetic element SCCmec carried by hospital-associated MRSA. The gene transcription product inhibits translation of a master regulator against S. aureus virulence genes, resulting in the attenuation of colony-spreading, exotoxin production, and animal killing ability.
{"title":"[Studies on the regulatory mechanism of Staphylococcus aureus virulence].","authors":"Chikara Kaito","doi":"10.3412/jsb.69.491","DOIUrl":"https://doi.org/10.3412/jsb.69.491","url":null,"abstract":"Staphylococcus aureus causes various diseases against humans, including skin infection, pneumonia, food poisoning, and meningitis. Methicillin-resistant S. aureus (MRSA) is resistant to a broad range of antibiotics, causing serious clinical problems. In this review, I summarize our studies to evaluate S. aureus virulence and identify novel virulence regulators. First, we utilized silkworms as an infection model of S. aureus and identified novel virulence factors of S. aureus. Some of the virulence factors interact with RNA in bacterial cells and regulate the expression of virulence factors. Second, we found that S. aureus cells spread on soft agar plates and form a giant colony. We call this phenomenon colony-spreading. High virulence community-acquired MRSA exhibits higher colony-spreading activity than hospital-associated MRSA. The difference in colony spreading is attributed to a specific gene in the mobile genetic element SCCmec carried by hospital-associated MRSA. The gene transcription product inhibits translation of a master regulator against S. aureus virulence genes, resulting in the attenuation of colony-spreading, exotoxin production, and animal killing ability.","PeriodicalId":19308,"journal":{"name":"Nihon saikingaku zasshi. Japanese journal of bacteriology","volume":"69 3","pages":"491-501"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3412/jsb.69.491","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32638755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Legionella are gram-negative bacteria ubiquitously found in freshwater and soil environments. Once inhaled by humans, Legionella infection could result in a severe form of pneumonia known as Legionellosis. Legionella translocate ~300 effector proteins into host cells via the Dot/Icm type IV secretion system, which is central to Legionella pathogenesis. Here I describe a brief review on recent advances in research on the molecular basis of Legionella-eukaryotic-cell interaction.
{"title":"[Host-pathogen interaction of Legionella pneumophila].","authors":"Hiroki Nagai","doi":"10.3412/jsb.69.503","DOIUrl":"https://doi.org/10.3412/jsb.69.503","url":null,"abstract":"<p><p>Legionella are gram-negative bacteria ubiquitously found in freshwater and soil environments. Once inhaled by humans, Legionella infection could result in a severe form of pneumonia known as Legionellosis. Legionella translocate ~300 effector proteins into host cells via the Dot/Icm type IV secretion system, which is central to Legionella pathogenesis. Here I describe a brief review on recent advances in research on the molecular basis of Legionella-eukaryotic-cell interaction. </p>","PeriodicalId":19308,"journal":{"name":"Nihon saikingaku zasshi. Japanese journal of bacteriology","volume":"69 3","pages":"503-11"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3412/jsb.69.503","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32638756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Spirochetes have flagella within the cell body and swim by wriggling the spiral cell body. Besides they have been known to be critical agents causing various infectious diseases, their eccentric appearances and motilities have been attracting many scientists in a wide variety of fields other than bacteriologists. Unlike externally flagellated bacteria that swim by using flagella as a screw propeller, spirochetes progress in a liquid by changing their cell shapes. To understand the unique motion mechanism of spirochetes, many experiments and theoretical studies are being carried out. In this review, I will summarize morphological and motile properties of various species of spirochete, such as Borrelia, Treponema and Brachyspira. I will also expound on the motion mechanism of Leptospira with our latest results obtained by high-resolution optical photometry.
{"title":"[Morphology and motility of the spirochetes].","authors":"Shuichi Nakamura","doi":"10.3412/jsb.69.527","DOIUrl":"https://doi.org/10.3412/jsb.69.527","url":null,"abstract":"<p><p>Spirochetes have flagella within the cell body and swim by wriggling the spiral cell body. Besides they have been known to be critical agents causing various infectious diseases, their eccentric appearances and motilities have been attracting many scientists in a wide variety of fields other than bacteriologists. Unlike externally flagellated bacteria that swim by using flagella as a screw propeller, spirochetes progress in a liquid by changing their cell shapes. To understand the unique motion mechanism of spirochetes, many experiments and theoretical studies are being carried out. In this review, I will summarize morphological and motile properties of various species of spirochete, such as Borrelia, Treponema and Brachyspira. I will also expound on the motion mechanism of Leptospira with our latest results obtained by high-resolution optical photometry. </p>","PeriodicalId":19308,"journal":{"name":"Nihon saikingaku zasshi. Japanese journal of bacteriology","volume":"69 3","pages":"527-38"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3412/jsb.69.527","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32638758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Bacteria show various cell shape such as round, rod, helical, and so on. However, each bacterium has its own shape and their length and width are kept in a narrow range in a population. Abnormal cell shape often results in death of the cells. Therefore, it is important to maintain their shape. Rod-shaped bacterium Escherichia coli needs to regulate cell polarity, length and width in order to form rod shape. Bacterial shape is genetically regulated. Especially, MreB, a bacterial actin, and its interacting proteins are involved in the regulation. We have identified rodZ as a novel cell shape determinant and have been analyzing RodZ protein in the past few years. The rodZ mutant is round. We isolated suppressor mutants of the rodZ mutant. The shape of the suppressors was rod shape. By analyzing the rodZ mutant and the suppressors, we concluded that RodZ helps assembly of MreB filaments. MreB plays roles in regulation of cell polarity, length, and width, whereas RodZ is involved in regulation of length and width. In this review, I summarize our research and research from other groups on bacterial cell shape.
{"title":"[Regulation of determination of bacterial shape].","authors":"Daisuke Shiomi","doi":"10.3412/jsb.69.557","DOIUrl":"https://doi.org/10.3412/jsb.69.557","url":null,"abstract":"<p><p>Bacteria show various cell shape such as round, rod, helical, and so on. However, each bacterium has its own shape and their length and width are kept in a narrow range in a population. Abnormal cell shape often results in death of the cells. Therefore, it is important to maintain their shape. Rod-shaped bacterium Escherichia coli needs to regulate cell polarity, length and width in order to form rod shape. Bacterial shape is genetically regulated. Especially, MreB, a bacterial actin, and its interacting proteins are involved in the regulation. We have identified rodZ as a novel cell shape determinant and have been analyzing RodZ protein in the past few years. The rodZ mutant is round. We isolated suppressor mutants of the rodZ mutant. The shape of the suppressors was rod shape. By analyzing the rodZ mutant and the suppressors, we concluded that RodZ helps assembly of MreB filaments. MreB plays roles in regulation of cell polarity, length, and width, whereas RodZ is involved in regulation of length and width. In this review, I summarize our research and research from other groups on bacterial cell shape. </p>","PeriodicalId":19308,"journal":{"name":"Nihon saikingaku zasshi. Japanese journal of bacteriology","volume":"69 4","pages":"557-64"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3412/jsb.69.557","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32857609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic infection with Helicobacter pylori is involved in a variety of clinical outcomes including gastric cancer. In the present study, we focused on the infection strategies of H. pylori associated with establishment of chronic infection. As a result, the following four findings revealed. 1) alpha-ketoglutarate oxidoreductase (KOR) is an essential survival enzyme for energy metabolism in the coccoid form of H. pylori, and inactivation of the KOR activity exerted a potent bactericidal action against H. pylori by preventing induction of the coccoid form. 2) SodB expression is derepressed by amino acids mutation of ferric uptake regulator (Fur), which is associated with the development of Metronidazole resistance. 3) FecA1 is an important determinant of the host-colonization ability through Fe(2+) supply to SodB, suggesting that FecA1 may be a possible target for the development of a novel bactericidal drug. 4) Intracellular CagA oncoprotein is degraded by autophagy and therefore short lived. However, in the CD44v9-expressing gastric cells, CagA specifically accumulated through the repression of autophagy induction.
{"title":"[Study of infection strategies of Helicobacter pylori and host cell response against CagA oncoprotein].","authors":"Hitoshi Tsugawa","doi":"10.3412/jsb.69.565","DOIUrl":"https://doi.org/10.3412/jsb.69.565","url":null,"abstract":"<p><p>Chronic infection with Helicobacter pylori is involved in a variety of clinical outcomes including gastric cancer. In the present study, we focused on the infection strategies of H. pylori associated with establishment of chronic infection. As a result, the following four findings revealed. 1) alpha-ketoglutarate oxidoreductase (KOR) is an essential survival enzyme for energy metabolism in the coccoid form of H. pylori, and inactivation of the KOR activity exerted a potent bactericidal action against H. pylori by preventing induction of the coccoid form. 2) SodB expression is derepressed by amino acids mutation of ferric uptake regulator (Fur), which is associated with the development of Metronidazole resistance. 3) FecA1 is an important determinant of the host-colonization ability through Fe(2+) supply to SodB, suggesting that FecA1 may be a possible target for the development of a novel bactericidal drug. 4) Intracellular CagA oncoprotein is degraded by autophagy and therefore short lived. However, in the CD44v9-expressing gastric cells, CagA specifically accumulated through the repression of autophagy induction. </p>","PeriodicalId":19308,"journal":{"name":"Nihon saikingaku zasshi. Japanese journal of bacteriology","volume":"69 4","pages":"565-75"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3412/jsb.69.565","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32857610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}