Flagellin of Enteropathogenic<i>Escherichia coli</i>Stimulates Interleukin-8 Production in T84 Cells

Zhou, Xin; Girón, Jorge A.; Torres, Alfredo G.; Crawford, J. Adam; Negrete, Erasmo; Vogel, Stefanie N.; Kaper, James B.

doi:10.1128/iai.71.4.2120-2129.2003

Cited by 128 publications

(137 citation statements)

References 59 publications

(67 reference statements)

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“…The amount of IL-8 released by Caco-2 cells due to complemented ⌬fliC EPEC was approximately 80% of the amount induced by WT EPEC infection. This finding is consistent with that of Zhou et al (47), who earlier reported partial restoration of IL-8 secretion from T84 IEC following complementation of flagellin-deficient EPEC. Our data indicate that flagellin is required for full induction of chemokine release from IEC.…”

Section: Vol 76 2008 Epithelial Responses To Epec and C Rodentium supporting

confidence: 93%

“…While the host response to these pathogens is not well understood, the increased expression of both chemokines, as well as antimicrobial peptides, has been detected in infected tissues (32,47). Our data suggest that the expression of these mediators during A/E pathogen infections may be initially due to epithelial cells.…”

Section: Discussionmentioning

confidence: 66%

“…Previous studies suggested that flagellin is the major factor within the EPEC supernatant that triggers IL-8 secretion from T84 human IEC (47). To determine if WT EPEC culture supernatant produces a similar response in LPShyporesponsive Caco-2 IEC, filter-sterilized bacterial culture supernatants were prepared from bacteria grown overnight in LB broth.…”

Section: Epec Supernatants Induce Il-8 Secretion From Caco-2 Cellsmentioning

confidence: 99%

“…Like lipopolysaccharide (LPS), flagellins contain pathogen-associated molecular patterns that are recognized by the innate immune system, triggering an inflammatory response (17). A study by Zhou et al demonstrated that flagellin is the major bacterial component responsible for the ability of EPEC supernatants to trigger IL-8 release from epithelial cells (47). Moreover, this inflammatory response required the activation of mitogen-activated protein kinases (MAPK), a group of serine-threonine kinases central to many host responses, including cytokine responses.…”

mentioning

confidence: 99%

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Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

Khan

Bouzari

et al. 2008

Infect Immun

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Enteropathogenic Escherichia coli (EPEC) and the murine pathogen Citrobacter rodentium belong to the attaching and effacing (A/E) family of bacterial pathogens. These noninvasive bacteria infect intestinal enterocytes using a type 3 secretion system (T3SS), leading to diarrheal disease and intestinal inflammation. While flagellin, the secreted product of the EPEC fliC gene, causes the release of interleukin 8 (IL-8) from epithelial cells, it is unclear whether A/E bacteria also trigger epithelial inflammatory responses that are FliC independent. The aims of this study were to characterize the FliC dependence or independence of epithelial inflammatory responses to direct infection by EPEC or C. rodentium. Following infection of Caco-2 intestinal epithelial cells by wild-type and ⌬fliC EPEC, a rapid activation of several proinflammatory genes, including those encoding IL-8, monocyte chemoattractant protein 1, macrophage inflammatory protein 3␣ (MIP3␣), and ␤-defensin 2, occurred in a FliC-dependent manner. These responses were accompanied by mitogen-activated protein kinase activation, as well as the Toll-like receptor 5 (TLR5)-dependent activation of NF-B. At later infection time points, a subset of these proinflammatory genes (IL-8 and MIP3␣) was also induced in cells infected with ⌬fliC EPEC. The nonmotile A/E pathogen C. rodentium also triggered similar innate responses through a TLR5-independent but partially NF-B-dependent mechanism. Moreover, the EPEC FliC-independent responses were increased in the absence of the locus of enterocyte effacement-encoded T3SS, suggesting that translocated bacterial effectors suppress rather than cause the FliC-independent inflammatory response. Thus, we demonstrate that infection of intestinal epithelial cells by A/E pathogens can trigger an array of proinflammatory responses from epithelial cells through both FliC-dependent and -independent pathways, expanding our understanding of the innate epithelial response to infection by these pathogens.

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Section: Vol 76 2008 Epithelial Responses To Epec and C Rodentium supporting

confidence: 93%

Section: Discussionmentioning

confidence: 66%

Section: Epec Supernatants Induce Il-8 Secretion From Caco-2 Cellsmentioning

confidence: 99%

mentioning

confidence: 99%

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Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

Khan

Bouzari

et al. 2008

Infect Immun

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“…Serovar Typhimurium can also translocate FliC across the intestinal epithelium in SPI-1-induced vesicles, where it stimulates a potent inflammatory response via Toll-like receptor 5 (TLR5) signaling (15). Proinflammatory chemokine production is also upregulated by FliC through TLR5 signaling during EHEC O157:H7 and EPEC O127:H6 infection of intestinal tissue (22,31,35). In addition to its involvement in inflammation, EPEC O127:H6 flagellin contributes to the adherence of bacteria to epithelial cells (16).…”

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confidence: 99%

Contribution of FliC to Epithelial Cell Invasion by Enterohemorrhagic Escherichia coli O113:H21

et al. 2006

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Enterohemorrhagic Escherichia coli (EHEC) O113:H21 can invade epithelial cells. In this study, we found that invasion but not adherence was inhibited by anti-FliC H21 specific antibodies. In addition, deletion of fliC H21 from EHEC O113:H21 resulted in an eightfold decrease in invasion that was restored upon transcomplementation with fliC H21 but not with fliC H6 . These results suggested that FliC plays an important role in the pathogenesis of infections caused by EHEC O113:H21 by allowing bacteria to penetrate the intestinal epithelium.Shiga toxin-producing Escherichia coli (STEC) strains associated with hemorrhagic colitis or the hemolytic-uremic syndrome (HUS) in humans are commonly referred to as enterohemorrhagic E. coli (EHEC) (32). Most EHEC strains carry the locus for enterocyte effacement (LEE), which is essential for intestinal colonization (12,14,19,27,34). Nevertheless, strains of EHEC that do not carry LEE are regularly isolated from patients with severe disease, and these isolates have been termed eae-or LEE-negative EHEC or STEC (2,4,11,13,17,20,24,25). We have shown previously that clinical isolates of LEE-negative EHEC have the ability to invade Chinese Hamster Ovary (CHO-K1) cells and the human colonic cell lines HCT-8 and Caco-2 (21). We speculate that this atypical subgroup of EHEC may use a mechanism of host cell invasion to colonize the intestinal mucosa.Recently, Rogers et al. used the streptomycin-treated mouse model to show that LEE-negative EHEC O113:H21 strain 98NK2 was closely associated with the colonic mucosa during infection (30). In addition, bacteria were observed to penetrate the gut epithelium, and this close interaction was dependent on fliC. Although there was no difference in the fecal shedding of wild-type 98NK2 and a 98NK2⌬fliC mutant, fliC was required for full lethality in mice mediated by Shiga toxin, suggesting that a close interaction of 98NK2 with the intestinal mucosa was important for virulence. In the present study, we have extended these findings to examine the contribution of FliC to invasion of HCT-8 epithelial cells by EHEC O113:H21.FliC H21 -mediated invasion of HCT-8 cells. Previous work has shown that FliC is more highly expressed at temperatures below 37°C in the invasive pathogens Yersinia enterocolitica and Listeria monocytogenes (3, 9, 18). We therefore examined FliC H21 expression by wild-type STEC O113:H21 strain EH41 at two different growth temperatures. EH41 is a clinical isolate that has been described previously (10). Bacteria were grown in Luria-Bertani (LB) broth to the same optical density (i.e., an optical density at 600 nm of 0.8 [mid-log phase]) at 25 and 37°C, and whole-cell lysates were analyzed by immunoblotting with anti-H21 antibodies (Statens Serum Institut, Copenhagen, Denmark). The results showed that FliC H21 production by EH41 was more abundant at 25°C than at 37°C (Fig. 1A). To determine whether increased expression of FliC H21 correlated with increased invasion, we performed invasion assays with EH41 grown in LB broth overnight ...

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Adherent-invasive Escherichia coli in inflammatory bowel disease

Rolhion¹,

Darfeuille‐Michaud²

2007

Inflammatory Bowel Diseases

225

164

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Increased numbers of mucosa-associated Escherichia coli are observed in both major inflammatory bowel diseases, Crohn's disease (CD) and ulcerative colitis (UC). With the identification of mutations in the NOD2-encoding gene in patients with CD and given the intracellular location of NOD2, the presence of pathogenic invasive bacteria could be the link between innate immune response to invasive bacteria and the development of the inflammation. Adherent-invasive E. coli (AIEC) are isolated from ileal biopsies of 36.4% of patients with ileal involvement of CD. These pathogenic E. coli colonize the intestinal mucosa by adhering to intestinal epithelial cells and are also true invasive pathogens, able to invade intestinal epithelial cells and to replicate intracellularly. AIEC strains also survive and replicate extensively within macrophages without inducing host cell death, and their high replication rates induce the secretion of large amounts of tumor necrosis factor alpha (TNF-alpha). There is also evidence suggesting that AIEC is involved in the formation of granulomas. The presence of AIEC is restricted to CD patients. Mucosa-associated E. coli in patients with UC can adhere to intestinal epithelial cells and induce the secretion of IL-8, but there is no evidence that these E. coli strains are invasive.

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Flagellin of EnteropathogenicEscherichia coliStimulates Interleukin-8 Production in T84 Cells

Cited by 128 publications

References 59 publications

Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

Contribution of FliC to Epithelial Cell Invasion by Enterohemorrhagic Escherichia coli O113:H21

Adherent-invasive Escherichia coli in inflammatory bowel disease

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