The Dependence of the
            <i>Yersinia</i>
            <i>pestis</i>
            Capsule on Pathogenesis Is Influenced by the Mouse Background

Weening, Eric H.; Cathelyn, Jason S.; Kaufman, Greer E.; Lawrenz, Matthew B.; Price, Paul A.; Goldman, William E.; Miller, Virginia L.

doi:10.1128/iai.00981-10

Cited by 40 publications

(48 citation statements)

References 41 publications

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“…inoculation than after s.c. inoculation. We previously demonstrated that after s.c. inoculation, Y. pestis deletion mutants lacking the transcriptional regulator RovA or the putative antiphagocytic factor PsaA are attenuated (20,27). Microarray and reverse transcription-quantitative PCR (qRT-PCR) analyses revealed that expression of psaA was substantially decreased in the ⌬rovA strain.…”

Section: Resultsmentioning

confidence: 99%

Comparison of Models for Bubonic Plague Reveals Unique Pathogen Adaptations to the Dermis

et al. 2015

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H ost-pathogen interactions begin with transmission and continue as the pathogen disseminates into deeper tissues. These tissues are in themselves microenvironments with defined immunological characteristics and can serve as barriers to prevent spread. For arthropod-borne pathogens, the skin epithelium is the first barrier that must be surpassed to penetrate into deeper organs (1, 2). The complexity of the immune responses of each layer of the skin reflects the specificity at which this tissue can act upon invaders.Based on its histological architecture, the skin can be divided into three main layers, namely, epidermis, dermis, and subcutaneous space (also known as hypodermis) (3). Each layer encompasses not only specific architectural qualities but also unique immunological characteristics that define them (2). How these characteristics influence the progression of infection is unknown. The epidermis is the outermost layer of the skin and constitutes a strong physical barrier that pathogens must cross to enter the body. Pathogens that survive in bloodfeeding arthropods can cross this layer through the mechanical action of the arthropod's probing mouth parts (4). Consequently, the dermis, located immediately adjacent to the epidermis, is highly exposed to these pathogens. Because most arthropod vectors do not penetrate beyond the dermis to the subcutaneous (s.c.) space, the dermis is, most likely, the first tissue where initial host-pathogen interactions occur during vector-borne infections (1,(5)(6)(7).Yersinia pestis is a Gram-negative bacterium and the causative agent of plague. This highly virulent pathogen was responsible for major pandemics in history and continues to survive in animal reservoirs in many parts of the world (8, 9). Bubonic plague is the most prevalent form of the disease and occurs after bacterial inoculation into the skin, typically by a flea vector (10). From the skin, Y. pestis disseminates to draining lymph nodes (LNs) via lymphatic vessels (11) and then to deeper organs through the bloodstream (12). Systemic dissemination results in septic shock, severe organ failure, and death.Models of infection that target the s.c. space are broadly used in plague research (13-16) as this is a relatively easy tissue to target. However, the dermis is strongly implicated as the layer of the skin probed by fleas during transmission (5, 17). In comparison with s.c. models, intradermal (i.d.) inoculations require more dexterity and can be more challenging to implement in biosafety level three facilities, which are mandatory when handling fully virulent strains of Y. pestis. In this study, we further characterize the i.d. model we used in a previous study (11) and compare i.d. and s.c. inoculations to investigate whether infection model impacts progression of bubonic plague. We found substantial differences in disease progression after inoculation by the two different routes. In addition, we found that dissemination of bacteria from the LNs is restricted. These findings are relevant for the understanding ...

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Section: Resultsmentioning

confidence: 99%

Comparison of Models for Bubonic Plague Reveals Unique Pathogen Adaptations to the Dermis

et al. 2015

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“…In a pneumonic plague model, animals infected with a ompX mutant of Y. pestis CO92 survived for two days longer than those infected with the parent strain (Kolodziejek et al, 2010). Moreover, Δcaf1 mutants and ΔpsaA mutants exhibited decreased virulence in a murine infection model (Weening et al, 2011). In a recent study, a Δcaf1 mutant of Y. pestis CO92 was attenuated for virulence in a mouse model of bubonic plague but not in a pneumonic plague mouse model when compared to the WT CO92 strain .…”

Section: Wwwintechopencommentioning

confidence: 99%

Recent Advancement in the Development of Vaccines Against Y. pestis - A Potential Agent of Bioterrorism

Ali¹,

Rao²

2012

Bioterrorism

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“…The F1 capsule, which is expressed at 37°C, is a major protective antigen of Y. pestis and forms a dense coating around the bacteria that prevents phagocytosis by host cells (10,13,17,24,49,60,67). The F1 capsule also has roles in transmission from the flea vector and contributes to pathogenesis in the mammalian host (61,73). Y. pestis also contains a third plasmid, pCD1, that is shared with enteropathogenic Yersinia spp.…”

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Roles of Chaperone/Usher Pathways of Yersinia pestis in a Murine Model of Plague and Adhesion to Host Cells

et al. 2012

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Yersinia pestis and many other Gram-negative pathogenic bacteria use the chaperone/usher (CU) pathway to assemble virulence-associated surface fibers termed pili or fimbriae. Y. pestis has two well-characterized CU pathways: the caf genes coding for the F1 capsule and the psa genes coding for the pH 6 antigen. The Y. pestis genome contains additional CU pathways that are capable of assembling pilus fibers, but the roles of these pathways in the pathogenesis of plague are not understood. We constructed deletion mutations in the usher genes for six of the additional Y. pestis CU pathways. The wild-type (WT) and usher deletion strains were compared in the murine bubonic (subcutaneous) and pneumonic (intranasal) plague infection models. Y. pestis strains containing deletions in CU pathways y0348-0352, y1858-1862, and y1869-1873 were attenuated for virulence compared to the WT strain by the intranasal, but not subcutaneous, routes of infection, suggesting specific roles for these pathways during pneumonic plague. We examined binding of the Y. pestis WT and usher deletion strains to A549 human lung epithelial cells, HEp-2 human cervical epithelial cells, and primary human and murine macrophages. Y. pestis CU pathways y0348-0352 and y1858-1862 were found to contribute to adhesion to all host cells tested, whereas pathway y1869-1873 was specific for binding to macrophages. The correlation between the virulence attenuation and host cell binding phenotypes of the usher deletion mutants identifies three of the additional CU pathways of Y. pestis as mediating interactions with host cells that are important for the pathogenesis of plague.

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The Dependence of the Yersinia pestis Capsule on Pathogenesis Is Influenced by the Mouse Background

Cited by 40 publications

References 41 publications

Comparison of Models for Bubonic Plague Reveals Unique Pathogen Adaptations to the Dermis

Comparison of Models for Bubonic Plague Reveals Unique Pathogen Adaptations to the Dermis

Recent Advancement in the Development of Vaccines Against Y. pestis - A Potential Agent of Bioterrorism

Roles of Chaperone/Usher Pathways of Yersinia pestis in a Murine Model of Plague and Adhesion to Host Cells

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