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Regulatory principles governing Salmonella and Yersinia virulence.

Erhardt M, Dersch P - Front Microbiol (2015)

Bottom Line: In order to manage sudden environmental changes, attacks by the host immune systems and microbial competition, the pathogens employ a plethora of transcriptional and post-transcriptional control elements, including transcription factors, sensory and regulatory RNAs, RNAses, and proteases, to fine-tune and control complex gene regulatory networks.However, the interplay, arrangement, and composition of the control elements vary between these closely related enteric pathogens, which generate phenotypic differences leading to distinct pathogenic properties.We highlight evolutionary changes of the gene regulatory circuits that result in different properties of the regulatory elements and how this influences the overall outcome of the infection process.

View Article: PubMed Central - PubMed

Affiliation: Young Investigator Group Infection Biology of Salmonella, Helmholtz Centre for Infection Research Braunschweig, Germany.

ABSTRACT
Enteric pathogens such as Salmonella and Yersinia evolved numerous strategies to survive and proliferate in different environmental reservoirs and mammalian hosts. Deciphering common and pathogen-specific principles for how these bacteria adjust and coordinate spatiotemporal expression of virulence determinants, stress adaptation, and metabolic functions is fundamental to understand microbial pathogenesis. In order to manage sudden environmental changes, attacks by the host immune systems and microbial competition, the pathogens employ a plethora of transcriptional and post-transcriptional control elements, including transcription factors, sensory and regulatory RNAs, RNAses, and proteases, to fine-tune and control complex gene regulatory networks. Many of the contributing global regulators and the molecular mechanisms of regulation are frequently conserved between Yersinia and Salmonella. However, the interplay, arrangement, and composition of the control elements vary between these closely related enteric pathogens, which generate phenotypic differences leading to distinct pathogenic properties. In this overview we present common and different regulatory networks used by Salmonella and Yersinia to coordinate the expression of crucial motility, cell adhesion and invasion determinants, immune defense strategies, and metabolic adaptation processes. We highlight evolutionary changes of the gene regulatory circuits that result in different properties of the regulatory elements and how this influences the overall outcome of the infection process.

No MeSH data available.


Related in: MedlinePlus

The course of infection by enteric Yersinia species and Salmonella enterica serovar Typhimurium. Enteropathogenic Salmonella Typhimurium utilizes flagellar motility for host colonization in the gut lumen and directed movement toward the epithelial layer. Salmonella attaches to the intestinal epithelium using a variety of adhesins and secretion of effector proteins via the Spi-1 encoded injectisome device for invasion of M cells or other enterocytes. The bacteria survive and replicate within Salmonella-containing vacuoles inside epithelial cells and phagocytes. The enteropathogenic Yersinia species Y. enterocolitica and Y. pseudotuberculosis are ingested via contaminated food and enter the lymphatic system through the M cells in the small intestine. In the lymphatic tissues they reside predominantly outside of the cells.
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Figure 1: The course of infection by enteric Yersinia species and Salmonella enterica serovar Typhimurium. Enteropathogenic Salmonella Typhimurium utilizes flagellar motility for host colonization in the gut lumen and directed movement toward the epithelial layer. Salmonella attaches to the intestinal epithelium using a variety of adhesins and secretion of effector proteins via the Spi-1 encoded injectisome device for invasion of M cells or other enterocytes. The bacteria survive and replicate within Salmonella-containing vacuoles inside epithelial cells and phagocytes. The enteropathogenic Yersinia species Y. enterocolitica and Y. pseudotuberculosis are ingested via contaminated food and enter the lymphatic system through the M cells in the small intestine. In the lymphatic tissues they reside predominantly outside of the cells.

Mentions: Enteric Yersinia and Salmonella serotypes are well adapted for survival in a variety of external environments and persistence in various host animals. The bacteria adjust rapidly to several extremely different and stressful environments during the invasion process, such as gastric acidity, increased osmolarity, changing nutrient/ion availability, and competition with the host’s microbiota in the intestine (Fabrega and Vila, 2013; Heroven and Dersch, 2014). In order to succeed in invading the host, they employ a wide variety of virulence factors, such as flagella, host colonization factors (fimbriae, adhesins/invasins), and many secreted toxins and effector proteins. These molecules are needed to propel the bacteria to target cells, attach to, infect and survive inside host cells and protect the pathogen against host immune responses (Figure 1). To establish a successful infection, process, these virulence factors and adequate metabolic pathways must be expressed at the correct spatiotemporal conditions. Consequently, a substantial cross-talk between different pathogenicity elements and physiological adaptation processes has to exist. The correct spatiotemporal expression of the various virulence constituents is achieved by regulation at the transcriptional, post-transcriptional and post-translational levels by a myriad of transcription factors, nucleoid-associated proteins, regulatory small RNAs (sRNAs) and RNases. Moreover, a growing set of small signaling molecules and different proteases controls the activity of enzymes and virulence-relevant factors during the infection process. The majority of the contributing regulators and control mechanisms are highly conserved between salmonellae and yersiniae, but the regulatory network composition and architecture are often changed. In the following chapters we will compare regulatory factors and global networks controlling early and late stages of the infection process of Salmonella and Yersinia to highlight conserved regulatory elements, but also changes that provided an important source for the divergence of the different genera with respect to their virulence-relevant physiological and pathogenic properties.


Regulatory principles governing Salmonella and Yersinia virulence.

Erhardt M, Dersch P - Front Microbiol (2015)

The course of infection by enteric Yersinia species and Salmonella enterica serovar Typhimurium. Enteropathogenic Salmonella Typhimurium utilizes flagellar motility for host colonization in the gut lumen and directed movement toward the epithelial layer. Salmonella attaches to the intestinal epithelium using a variety of adhesins and secretion of effector proteins via the Spi-1 encoded injectisome device for invasion of M cells or other enterocytes. The bacteria survive and replicate within Salmonella-containing vacuoles inside epithelial cells and phagocytes. The enteropathogenic Yersinia species Y. enterocolitica and Y. pseudotuberculosis are ingested via contaminated food and enter the lymphatic system through the M cells in the small intestine. In the lymphatic tissues they reside predominantly outside of the cells.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4563271&req=5

Figure 1: The course of infection by enteric Yersinia species and Salmonella enterica serovar Typhimurium. Enteropathogenic Salmonella Typhimurium utilizes flagellar motility for host colonization in the gut lumen and directed movement toward the epithelial layer. Salmonella attaches to the intestinal epithelium using a variety of adhesins and secretion of effector proteins via the Spi-1 encoded injectisome device for invasion of M cells or other enterocytes. The bacteria survive and replicate within Salmonella-containing vacuoles inside epithelial cells and phagocytes. The enteropathogenic Yersinia species Y. enterocolitica and Y. pseudotuberculosis are ingested via contaminated food and enter the lymphatic system through the M cells in the small intestine. In the lymphatic tissues they reside predominantly outside of the cells.
Mentions: Enteric Yersinia and Salmonella serotypes are well adapted for survival in a variety of external environments and persistence in various host animals. The bacteria adjust rapidly to several extremely different and stressful environments during the invasion process, such as gastric acidity, increased osmolarity, changing nutrient/ion availability, and competition with the host’s microbiota in the intestine (Fabrega and Vila, 2013; Heroven and Dersch, 2014). In order to succeed in invading the host, they employ a wide variety of virulence factors, such as flagella, host colonization factors (fimbriae, adhesins/invasins), and many secreted toxins and effector proteins. These molecules are needed to propel the bacteria to target cells, attach to, infect and survive inside host cells and protect the pathogen against host immune responses (Figure 1). To establish a successful infection, process, these virulence factors and adequate metabolic pathways must be expressed at the correct spatiotemporal conditions. Consequently, a substantial cross-talk between different pathogenicity elements and physiological adaptation processes has to exist. The correct spatiotemporal expression of the various virulence constituents is achieved by regulation at the transcriptional, post-transcriptional and post-translational levels by a myriad of transcription factors, nucleoid-associated proteins, regulatory small RNAs (sRNAs) and RNases. Moreover, a growing set of small signaling molecules and different proteases controls the activity of enzymes and virulence-relevant factors during the infection process. The majority of the contributing regulators and control mechanisms are highly conserved between salmonellae and yersiniae, but the regulatory network composition and architecture are often changed. In the following chapters we will compare regulatory factors and global networks controlling early and late stages of the infection process of Salmonella and Yersinia to highlight conserved regulatory elements, but also changes that provided an important source for the divergence of the different genera with respect to their virulence-relevant physiological and pathogenic properties.

Bottom Line: In order to manage sudden environmental changes, attacks by the host immune systems and microbial competition, the pathogens employ a plethora of transcriptional and post-transcriptional control elements, including transcription factors, sensory and regulatory RNAs, RNAses, and proteases, to fine-tune and control complex gene regulatory networks.However, the interplay, arrangement, and composition of the control elements vary between these closely related enteric pathogens, which generate phenotypic differences leading to distinct pathogenic properties.We highlight evolutionary changes of the gene regulatory circuits that result in different properties of the regulatory elements and how this influences the overall outcome of the infection process.

View Article: PubMed Central - PubMed

Affiliation: Young Investigator Group Infection Biology of Salmonella, Helmholtz Centre for Infection Research Braunschweig, Germany.

ABSTRACT
Enteric pathogens such as Salmonella and Yersinia evolved numerous strategies to survive and proliferate in different environmental reservoirs and mammalian hosts. Deciphering common and pathogen-specific principles for how these bacteria adjust and coordinate spatiotemporal expression of virulence determinants, stress adaptation, and metabolic functions is fundamental to understand microbial pathogenesis. In order to manage sudden environmental changes, attacks by the host immune systems and microbial competition, the pathogens employ a plethora of transcriptional and post-transcriptional control elements, including transcription factors, sensory and regulatory RNAs, RNAses, and proteases, to fine-tune and control complex gene regulatory networks. Many of the contributing global regulators and the molecular mechanisms of regulation are frequently conserved between Yersinia and Salmonella. However, the interplay, arrangement, and composition of the control elements vary between these closely related enteric pathogens, which generate phenotypic differences leading to distinct pathogenic properties. In this overview we present common and different regulatory networks used by Salmonella and Yersinia to coordinate the expression of crucial motility, cell adhesion and invasion determinants, immune defense strategies, and metabolic adaptation processes. We highlight evolutionary changes of the gene regulatory circuits that result in different properties of the regulatory elements and how this influences the overall outcome of the infection process.

No MeSH data available.


Related in: MedlinePlus