The Enteropathogenic E. coli Effector EspB Facilitates Microvillus Effacing and Antiphagocytosis by Inhibiting Myosin Function

Iizumi, Yosuke; Sagara, Hiroshi; Kabe, Yoshio; Azuma, Motoki; Kume, Kanako; Ogawa, Michinaga; Nagai, Takeshi; Gillespie, Peter G.; Sasakawa, Chihiro; Handa, Hiroshi

doi:10.1016/j.chom.2007.09.012

Cited by 93 publications

(86 citation statements)

References 31 publications

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“…The decrease in transepithelial electrical resistance is largely due to perturbations in the apical junctional complex mediated by the EPEC and enterohemorragic E. coli type III secretion system effector protein EspF (95,144). More recently, another EPEC effector protein, EspB, was shown to be critical for the microvillus effacing and inhibition of phagocytosis that is induced by EPEC infection (56).…”

Section: Epithelial Cell Interactions With Pathogensmentioning

confidence: 99%

Bacteria in the Intestine, Helpful Residents or Enemies from Within?

2008

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Section: Epithelial Cell Interactions With Pathogensmentioning

confidence: 99%

Bacteria in the Intestine, Helpful Residents or Enemies from Within?

2008

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“…Microvillus effacement activity of the tEPEC protein EspF in the Caco-2/TC7 cells was dependent on its N-WASP binding motif (93). EspB binds to myosin and blocks its interaction with actin in fully differentiated Caco-2 cells (607). tEPEC uses the clathrincoated pit components Eps15 and epsin1, but not adaptor protein 2 (AP-2), in clathrin-dependent pedestal formation in fully differentiated Caco-2 cells (608).…”

Section: Structural and Functional Injuriesmentioning

confidence: 99%

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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“…EspB plays a central role in pathogenesis both by its membrane lytic and its myosin-binding functions. EspB is responsible for microvillus distortion and close bacterial attachment (the attaching and effacing lesion) [42]. Studies using purified EspB demonstrated that human recombinant lactoferrin has a direct proteolytic effect on EspB that can be prevented by serine pro-tease inhibitors.…”

Section: Enteropathogenic E Coli (Epec)mentioning

confidence: 99%

Effect of lactoferrin on enteric pathogens

Ochoa

Cleary²

2009

Biochimie

119

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Much has been learned in recent years about the mechanisms by which breastfeeding improves child health and survival. However, there has been little progress in using these insights to improve pediatric care. Factors that are important for protecting the breast fed infant might be expected to decrease the adverse effects of weaning on diarrhea, growth, and development. Lactoferrin, an ironbinding protein with multiple physiological functions (anti-microbial, anti-inflammatory, and immunomodulatory), is one of the most important proteins present in mammalian milk. Protection against gastroenteritis is the most likely biologically relevant activity of lactoferrin. Multiple in vitro and animal studies have shown a protective effect of lactoferrin on infections with enteric microorganisms, including rotavirus, Giardia, Shigella, Salmonella and the diarrheagenic Escherichia coli. Lactoferrin has two major effects on enteric pathogens: it inhibits growth and it impairs function of surface expressed virulence factors thereby decreasing their ability to adhere or to invade mammalian cells. Thus, lactoferrin may protect infants from gastrointestinal infection by preventing the attachment by enteropathogens in the gut. Recently several clinical trials in children have started to address this issue. Whether lactoferrin can prevent a significant portion of diarrheal disease remains to be determined.

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The Enteropathogenic E. coli Effector EspB Facilitates Microvillus Effacing and Antiphagocytosis by Inhibiting Myosin Function

Cited by 93 publications

References 31 publications

Bacteria in the Intestine, Helpful Residents or Enemies from Within?

Bacteria in the Intestine, Helpful Residents or Enemies from Within?

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

Effect of lactoferrin on enteric pathogens

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