Flagellin in combination with curli fimbriae elicits an immune response in the gastrointestinal epithelial cell line HT-29

Rochon, Maike; Römling, Ute

doi:10.1016/j.micinf.2006.03.003

Cited by 16 publications

(16 citation statements)

References 42 publications

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“…The expression of biofilm matrix components in Enterobacteria alters the interaction of microorganisms with its host (Ledeboer and Jones, 2005;Rochon and Romling, 2006). In the case of Nissle 1917, cellulose production affected host cell attachment and invasion, and IL-8 production by the host cells ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Characterization of cellulose production in Escherichia coli Nissle 1917 and its biological consequences

Monteiro

Saxena

Xiao-da

et al. 2009

Environmental Microbiology

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Bacterial species of the Enterobacteriaceae family produce cellulose and curli fimbriae as extracellular matrix components, and their synthesis is positively regulated by the transcriptional activator CsgD. In this group of bacteria, cellulose biosynthesis is commonly regulated by CsgD via the GGDEF domain protein AdrA, a diguanylate cyclase that produces cyclic-diguanylic acid (c-di-GMP), an allosteric activator of cellulose synthase. In the probiotic Escherichia coli strain Nissle 1917 and its recent clonal isolates, CsgD activates the production of curli fimbriae at 28 degrees C, but neither CsgD nor AdrA is required for the c-di-GMP-dependent biosynthesis of cellulose at 28 degrees C and 37 degrees C. In these strains, the GGDEF domain protein YedQ, a diguanylate cyclase that activates cellulose biosynthesis in certain E. coli strains, is not required for cellulose biosynthesis and it has in fact evolved into a novel protein. Cellulose production in Nissle 1917 is required for adhesion of bacteria to the gastrointestinal epithelial cell line HT-29, to the mouse epithelium in vivo, and for enhanced cytokine production. The role of cellulose in this strain is in contrast to the role of cellulose in the commensal strain E. coli TOB1. Consequently, the role of cellulose in bacterial-host interaction is dependent on the E. coli strain background.

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Section: Discussionmentioning

confidence: 99%

Characterization of cellulose production in Escherichia coli Nissle 1917 and its biological consequences

Monteiro

Saxena

Xiao-da

et al. 2009

Environmental Microbiology

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“…Previous studies showed that flagellin is secreted into the medium by the flagella secretory apparatus during flagella biosynthesis, in amounts sufficient to cause a proinflammatory immune response. [39][40] Other reports speculated that monomeric or oligomeric flagellin could be also released by the action of proteolytic enzymes, bile salts, or surfactants present in mucosal sites. 41 Moreover, evidence for the release of proinflammatory flagellin monomers in vivo was recently reported by Subramanian and Qadri 42 , who showed that not only the interaction of Salmonella and intestinal epithelial cells promoted monomeric flagellin release but also that this flagellin was not derived from shearing or depolymerization of flagella present on the surface of the bacterium but instead was newly synthesized and secreted after bacterial sensing of host-produced lysophospholipids.…”

Section: Discussionmentioning

confidence: 99%

Flagellin delays spontaneous human neutrophil apoptosis

Salamone

Petracca

Bass

et al. 2010

Laboratory Investigation

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Neutrophils are short-lived cells that rapidly undergo apoptosis. However, their survival can be regulated by signals from the environment. Flagellin, the primary component of the bacterial flagella, is known to induce neutrophil activation. In this study we examined the ability of flagellin to modulate neutrophil apoptosis. Neutrophils cultured for 12 and 24 h in the presence of flagellin from Salmonella thyphimurim at concentrations found in pathological situations underwent a marked prevention of apoptosis. In contrast, Helicobacter pylori flagellin did not affect neutrophil survival, suggesting that Salmonella flagellin exerts the antiapoptotic effect by interacting with TLR5. The delaying in apoptosis mediated by Salmonella flagellin was coupled to higher expression levels of the antiapoptotic protein Mcl-1 and lower levels of activated caspase-3. Analysis of the signaling pathways indicated that Salmonella flagellin induced the activation of the p38 and ERK1/2 MAPK pathways as well as the PI3K/Akt pathway. Furthermore, it also stimulated IkBa degradation and the phosphorylation of the p65 subunit, suggesting that Salmonella flagellin also triggers NF-kB activation. Moreover, the pharmacological inhibition of ERK1/2 pathway and NF-kB activation partially prevented the antiapoptotic effects exerted by flagellin. Finally, the apoptotic delaying effect exerted by flagellin was also evidenced when neutrophils were cultured with whole heat-killed S. thyphimurim. Both a wild-type and an aflagellate mutant S. thyphimurim strain promoted neutrophil survival; however, when cultured in low bacteria/neutrophil ratios, the flagellate bacteria showed a higher capacity to inhibit neutrophil apoptosis, although both strains showed a similar ability to induce neutrophil activation. Taken together, our results indicate that flagellin delays neutrophil apoptosis by a mechanism partially dependent on the activation of ERK1/2 MAPK and NF-kB. The ability of flagellin to delay neutrophil apoptosis could contribute to perpetuate the inflammation during infections with flagellated bacteria.

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“…The flagellar filament of S. enterica is comprised of two antigenically distinct subunit proteins, FliC (H:i) and FljB (H:1,2), and this is a pathogen-associated molecular pattern detected by mammalian cells via surface-expressed Toll-like receptor 5 and cytosolic Nod-like receptors (30,80). Secretion of interleukin-1␤ by mouse cell lines is activated comparably by the FliC and FljB flagellins (88), but memory CD4 ϩ T cells preferentially recognize FliC during adaptive immunity and Salmonella committed to expressing only FljB is attenuated in vivo (8,41).…”

Section: Vol 192 2010mentioning

confidence: 99%

Flagellated but Not Hyperfimbriated Salmonella enterica Serovar Typhimurium Attaches to and Forms Biofilms on Cholesterol-Coated Surfaces

2010

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The asymptomatic, chronic carrier state of Salmonella enterica serovar Typhi occurs in the bile-rich gallbladder and is frequently associated with the presence of cholesterol gallstones. We have previously demonstrated that salmonellae form biofilms on human gallstones and cholesterol-coated surfaces in vitro and that bile-induced biofilm formation on cholesterol gallstones promotes gallbladder colonization and maintenance of the carrier state. Random transposon mutants of S. enterica serovar Typhimurium were screened for impaired adherence to and biofilm formation on cholesterol-coated Eppendorf tubes but not on glass and plastic surfaces. We identified 49 mutants with this phenotype. The results indicate that genes involved in flagellum biosynthesis and structure primarily mediated attachment to cholesterol. Subsequent analysis suggested that the presence of the flagellar filament enhanced binding and biofilm formation in the presence of bile, while flagellar motility and expression of type 1 fimbriae were unimportant. Purified Salmonella flagellar proteins used in a modified enzyme-linked immunosorbent assay (ELISA) showed that FliC was the critical subunit mediating binding to cholesterol. These studies provide a better understanding of early events during biofilm development, specifically how salmonellae bind to cholesterol, and suggest a target for therapies that may alleviate biofilm formation on cholesterol gallstones and the chronic carrier state.

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Flagellin in combination with curli fimbriae elicits an immune response in the gastrointestinal epithelial cell line HT-29

Cited by 16 publications

References 42 publications

Characterization of cellulose production in Escherichia coli Nissle 1917 and its biological consequences

Characterization of cellulose production in Escherichia coli Nissle 1917 and its biological consequences

Flagellin delays spontaneous human neutrophil apoptosis

Flagellated but Not Hyperfimbriated Salmonella enterica Serovar Typhimurium Attaches to and Forms Biofilms on Cholesterol-Coated Surfaces

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