A Rationale for Repression and/or Loss of Motility by Pathogenic Yersinia in the Mammalian Host

Minnich, Scott A.; Rohde, Harold N.

doi:10.1007/978-0-387-72124-8_27

Cited by 52 publications

(55 citation statements)

References 25 publications

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“…It is well established that Y. enterocolitica flagella are downregulated at 37°C, likely as an adaptation to avoid being recognized by Toll-like receptor 5 (TLR5) (18). This expected result confirms the utility of our technique in discovering systems that are differentially expressed upon changing environmental conditions.…”

Section: Resultssupporting

confidence: 70%

“…Bacteria must also repress the expression of genes that provide no advantage or constitute a disadvantage in the host environment. Genes that encode proteins like FliC, which is easily detected by the host immune system, fall into this category (18). Among the most important virulence factors expressed by nearly all bacterial pathogens are the secretion systems.…”

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confidence: 99%

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Transcriptomic Analysis of Yersinia enterocolitica Biovar 1B Infecting Murine Macrophages Reveals New Mechanisms of Extracellular and Intracellular Survival

et al. 2015

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c Yersinia enterocolitica is typically considered an extracellular pathogen; however, during the course of an infection, a significant number of bacteria are stably maintained within host cell vacuoles. Little is known about this population and the role it plays during an infection. To address this question and to elucidate the spatially and temporally dynamic gene expression patterns of Y. enterocolitica biovar 1B through the course of an in vitro infection, transcriptome sequencing and differential gene expression analysis of bacteria infecting murine macrophage cells were performed under four distinct conditions. Bacteria were first grown in a nutrient-rich medium at 26°C to establish a baseline of gene expression that is unrelated to infection. The transcriptomes of these bacteria were then compared to bacteria grown in a conditioned cell culture medium at 37°C to identify genes that were differentially expressed in response to the increased temperature and medium but not in response to host cells. Infections were then performed, and the transcriptomes of bacteria found on the extracellular surface and intracellular compartments were analyzed individually. The upregulated genes revealed potential roles for a variety of systems in promoting intracellular virulence, including the Ysa type III secretion system, the Yts2 type II secretion system, and the Tad pilus. It was further determined that mutants of each of these systems had decreased virulence while infecting macrophages. Overall, these results reveal the complete set of genes expressed by Y. enterocolitica in response to infection and provide the groundwork for future virulence studies.T he genus Yersinia includes three species that are pathogenic to humans: Y. pestis, the causative agent of the plague, as well as Y. enterocolitica and Y. pseudotuberculosis, both of which cause gastrointestinal diseases. Of the three organisms, Y. enterocolitica is the species most frequently isolated from humans (1). Y. enterocolitica infections are typically acquired through ingestion of the bacteria in contaminated food or water, especially raw or undercooked pork products (2). After ingestion, the bacteria travel through the gastrointestinal tract to the terminal ileum, where they are able to penetrate the M cells of the Peyer's patches and infect the mesenteric lymph nodes (1-3). This leads to a self-limiting gastroenteritis and mesenteric lymphadenitis in otherwise healthy patients (3). In immunocompromised patients or young children with developing immune systems, the bacteria can spread from the lymph nodes to systemic sites, leading to potentially fatal septicemia (1). Over half of all reported Y. enterocolitica infections occur in children under the age of five, the group that is most predisposed to developing the systemic form of the infection (4).Pathogenic Y. enterocolitica isolates can be divided into six distinct biovars based on several biochemical and physiological attributes (2, 5). Of the six biovars, the North American isolate, biovar 1B, is the most...

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Section: Resultssupporting

confidence: 70%

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confidence: 99%

Transcriptomic Analysis of Yersinia enterocolitica Biovar 1B Infecting Murine Macrophages Reveals New Mechanisms of Extracellular and Intracellular Survival

et al. 2015

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“…However, it is possible that C. difficile represses the expression of the fliC and fliD genes, and therefore motility, upon the infection of its host and that this is part of its pathogenic strategy. For example, Yersinia enterocolitica represses flagellum expression in its mammalian host, a mechanism that is thought to allow the organism to evade the host's innate immune system (21). Conversely, artificial expression of flagellin in Y. enterocolitica results in complete attenuation of virulence in a mouse model of infection (21).…”

Section: Discussionmentioning

confidence: 99%

Mutagenic Analysis of the Clostridium difficile Flagellar Proteins, FliC and FliD, and Their Contribution to Virulence in Hamsters

2011

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Although toxins A and B are known to be important contributors to the acute phase of Clostridium difficile infection, the role of colonization and adherence to host tissues in the overall pathogenesis of these organisms remains unclear. Consequently, we used the recently introduced intron-based ClosTron gene interruption system to eliminate the expression of two reported C. difficile colonization factors, the major flagellar structural subunit (FliC) and the flagellar cap protein (FliD), to gain greater insight into how flagella and motility contribute to C. difficile's pathogenic strategy. The results demonstrate that interrupting either the fliC or the fliD gene results in a complete loss of flagella, as well as motility, in C. difficile. However, both the fliC and fliD mutant strains adhered better than the wild-type 630⌬erm strain to human intestine-derived Caco-2 cells, suggesting that flagella and motility do not contribute to, or may even interfere with, C. difficile adherence to epithelial cell surfaces in vitro. Moreover, we found that the mutant strains were more virulent in hamsters, indicating either that flagella are unnecessary for virulence or that repression of motility may be a pathogenic strategy employed by C. difficile in hamsters.

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“…CheY is well studied in Salmonella and E. coli regarding its role in motility signal transduction via flagellar rotation (53). Given that Y. pestis is nonmotile and that loss of motility is thought to enhance innate immune evasion by loss of flagellin expression (33), the role of CheY is enigmatic. However, we were able to detect cheY transcripts in KIM5 using real-time RT-PCR (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Yersinia pestisTwo-Component Gene Regulatory Systems Promote Survival in Human Neutrophils

et al. 2010

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A Rationale for Repression and/or Loss of Motility by Pathogenic Yersinia in the Mammalian Host

Cited by 52 publications

References 25 publications

Transcriptomic Analysis of Yersinia enterocolitica Biovar 1B Infecting Murine Macrophages Reveals New Mechanisms of Extracellular and Intracellular Survival

Transcriptomic Analysis of Yersinia enterocolitica Biovar 1B Infecting Murine Macrophages Reveals New Mechanisms of Extracellular and Intracellular Survival

Mutagenic Analysis of the Clostridium difficile Flagellar Proteins, FliC and FliD, and Their Contribution to Virulence in Hamsters

Yersinia pestisTwo-Component Gene Regulatory Systems Promote Survival in Human Neutrophils

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