Fimbrial Polyadhesins: Anti-immune Armament of Yersinia

Zav’yalov, Vladimir P.

doi:10.1007/978-1-4614-3561-7_24

Cited by 4 publications

(1 citation statement)

References 91 publications

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“…Pathogenic Yersinia produce numerous surface located proteins that could possess auto-agglutinating properties, engage with host cell surface receptors or act as serum resistance factors that limit the action of complement-mediated opsonization and killing (Figure 1 ). The most prominent Yersinia adhesins studied to date are invasin, YadA, Ail, and pH 6 antigen (Kolodziejek et al, 2012 ; Zav'yalov, 2012 ; Mikula et al, 2013 ; Muhlenkamp et al, 2015 ). However, their relative importance to the biology of infection is pathogen-dependent, and in certain cases may not be required at all.…”

Section: Yersinia Biology and Classical Virulence Traitsmentioning

confidence: 99%

Environmental Regulation of Yersinia Pathophysiology

Chen

Thompson

Francis

2016

Front. Cell. Infect. Microbiol.

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Hallmarks of Yersinia pathogenesis include the ability to form biofilms on surfaces, the ability to establish close contact with eukaryotic target cells and the ability to hijack eukaryotic cell signaling and take over control of strategic cellular processes. Many of these virulence traits are already well-described. However, of equal importance is knowledge of both confined and global regulatory networks that collaborate together to dictate spatial and temporal control of virulence gene expression. This review has the purpose to incorporate historical observations with new discoveries to provide molecular insight into how some of these regulatory mechanisms respond rapidly to environmental flux to govern tight control of virulence gene expression by pathogenic Yersinia.

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Section: Yersinia Biology and Classical Virulence Traitsmentioning

confidence: 99%

Environmental Regulation of Yersinia Pathophysiology

Chen

Thompson

Francis

2016

Front. Cell. Infect. Microbiol.

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Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Moal

Servin

2013

Microbiol Mol Biol Rev

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SUMMARY Hosts are protected from attack by potentially harmful enteric microorganisms, viruses, and parasites by the polarized fully differentiated epithelial cells that make up the epithelium, providing a physical and functional barrier. Enterovirulent bacteria interact with the epithelial polarized cells lining the intestinal barrier, and some invade the cells. A better understanding of the cross talk between enterovirulent bacteria and the polarized intestinal cells has resulted in the identification of essential enterovirulent bacterial structures and virulence gene products playing pivotal roles in pathogenesis. Cultured animal cell lines and cultured human nonintestinal, undifferentiated epithelial cells have been extensively used for understanding the mechanisms by which some human enterovirulent bacteria induce intestinal disorders. Human colon carcinoma cell lines which are able to express in culture the functional and structural characteristics of mature enterocytes and goblet cells have been established, mimicking structurally and functionally an intestinal epithelial barrier. Moreover, Caco-2-derived M-like cells have been established, mimicking the bacterial capture property of M cells of Peyer's patches. This review intends to analyze the cellular and molecular mechanisms of pathogenesis of human enterovirulent bacteria observed in infected cultured human colon carcinoma enterocyte-like HT-29 subpopulations, enterocyte-like Caco-2 and clone cells, the colonic T84 cell line, HT-29 mucus-secreting cell subpopulations, and Caco-2-derived M-like cells, including cell association, cell entry, intracellular lifestyle, structural lesions at the brush border, functional lesions in enterocytes and goblet cells, functional and structural lesions at the junctional domain, and host cellular defense responses.

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Adhesines of the Plague Agent

Куклева¹

2018

Problemy Osobo Opasnykh Infektsii

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удк 616.98:579.842.23 л.м.куклева адгеЗинЫ воЗБудителя чумЫ ФКУЗ «Российский научно-исследовательский противочумный институт «Микроб», Саратов, Российская Федерация возбудитель чумы обладает комплексом адгезинов, обеспечивающих прикрепление возбудителя к клеткам-мишеням в организме хозяина и во многом определяющих начало, характер и течение болезни. наличие адгези-нов обеспечивает транслокацию эффекторных белков в клетки-мишени млекопитающих. в обзоре представлены литературные данные как о наиболее изученных адгезинах Yersinia pestis (белках Ail и pH6 антиген), так и о недавно выявленных аутотранспортных белках различных классов, участвующих в процессах адгезии (YadBC, Yaps, Ilp). описано их значение для патогенеза чумы, генетическая детерминированность, структура и локализа-ция в клетке. отмечено, что адгезины возбудителя чумы действуют на разных стадиях инфекционного процесса, выполняют множественные функции, участвуют не только в процессах прикрепления к клеткам хозяина, но так-же обеспечивают устойчивость к действию иммунных механизмов хозяина.Ключевые слова: возбудитель чумы, адгезины, патогенность.

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Fimbrial Polyadhesins: Anti-immune Armament of Yersinia

Cited by 4 publications

References 91 publications

Environmental Regulation of Yersinia Pathophysiology

Environmental Regulation of Yersinia Pathophysiology

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Adhesines of the Plague Agent

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