Virulence of Campylobacter species: A molecular genetic approach

Ketley, Julian M.

doi:10.1099/00222615-42-5-312

Cited by 40 publications

(28 citation statements)

References 121 publications

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“…All the C. jejuni isolates were detected in the lower chamber after incubation for 1 h, as reported by Konkel et al [ll], and continued to translocate for up to 6 h as noted previously by Ketley [8]. Isolate no.…”

Section: Discussionsupporting

confidence: 60%

“…This model has been used to investigate epithelial cell translocation for a number of pathogens including Salmonella spp. [5] and C. jejuni [ 1 1, 181. Although previous studies have demonstrated the ability of C. jejuni to translocate across Caco-2 cell monolayers [8,11,191, neither the mechanism by which campylobacters invades these cells, nor the relative contribution of paracellular translocation to epithelial penetration in these systems is completely understood. Previous studies [ 181 have demonstrated that more invasive and translocating strains may correspond to those that cause colitis and more severe disease.…”

Section: Introductionmentioning

confidence: 99%

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Different invasion phenotypes of Campylobacter isolates in Caco-2 cell monolayers

Harvey¹,

Battle²,

Leach³

1999

Journal of Medical Microbiology

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The pathogenesis of campylobacter enteritis is not well understood, but invasion into and translocation across intestinal epithelial cells may be involved in the disease process, as demonstrated for a number of other enteric pathogens. However, the mechanisms involved in these processes are not clearly defined for campylobacters. In this study, isolates were compared quantitatively in established assays with the enterocyte-like cell line, Caco-2, to determine the extent to which intracellular invasion contributes to translocation across epithelial cell monolayers, and whether isolates vary in this respect. Ten fresh Campylobacter isolates were compared and shown to differ in invasiveness by a factor of 10-fold by following their recovery from gentamicin-treated Caco-2 cells grown on nonpermeable tissue-culture wells. Four of these isolates with contrasting invasive ability were also shown to vary in their ability to translocate across Caco-2 cells grown on semipermeable Transwell inserts by a factor > 10. However, translocation did not quantitatively correlate with the intracellular invasiveness of these isolates. Isolate no. 9752 was poorly invasive but had modest translocation ability, isolate no. 10392 was very invasive but did not translocate significantly and remained within the monolayer, isolate no. 9519 both translocated and invaded well, whereas, isolate no. 235 translocated very efficiently but was poorly invasive. Isolate no. 9519 also uniquely caused a transitory flattening of the Caco-2 cells and a possible drop in trans-epithelial electrical resistance (TEER) of the Transwell monolayers, whereas isolate no. 235 did not show these effects. Together these data demonstrate that there are significantly different 'invasion' phenotypes among Campylobacter strains involving different degrees of intracellular invasion, and either different rates of transcellular trafficking or, alternatively, paracellular trafficking.

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Section: Discussionsupporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

Different invasion phenotypes of Campylobacter isolates in Caco-2 cell monolayers

Harvey¹,

Battle²,

Leach³

1999

Journal of Medical Microbiology

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“…A series of shuttle vectors have been constructed that contain both E. coli and C. coli origins of replication and Campylobacter-derived antibiotic resistance genes (Labigne-Roussel et af., 1987;Wang & Taylor, 1990a, b; Purdy & Park, 1993;Yao et al, 1993). The identification of genes and particularly of those unique to the campylobacters is even more difficult due to the fact that transposons of either Gram-negative or Grampositive origin or ' recombinant ' transposons (Ketley, 1995) have not been found to transpose in campylobacters. Genetic transformation, albeit at a low frequency, can be carried out by electroporation (Miller et al, 1988).…”

Section: Campylobacter Biologymentioning

confidence: 99%

“…It has been speculated that, like N . gonorrhoeae, the SOS response system of C. jejuni may have evolved to increase the chance of recombining exogenous DNA whilst avoiding the initiation of the SOS response (Ketley , 1995).…”

Section: Campylobacter Biologymentioning

confidence: 99%

Pathogenesis of Enteric Infection by Campylobacter

1997

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“…process (17,18,32,33). However, bacterial internalization has typically been observed to involve rearrangement of the host cytoskeletal structure, resulting in endocytosis of the pathogen (10,14,16).…”

mentioning

confidence: 99%

Infection with Campylobacter jejuni Induces Tyrosine‐Phosphorylated Proteins into INT‐407 Cells

Biswas

Niwa

Itoh

2004

Microbiology and Immunology

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The mechanisms used by Campylobacter jejuni to induce internalization into host intestinal epithelial cells have not been defined. In this study, we obtained evidence that exposure of INT‐407 cells to protein kinase inhibitors results in decreased invasion of these cells by C. jejuni in a dose dependent manner. Preincubation of INT‐407 cells in the presence of staurosporine, tyrphostin 46 and genistein decreased invasion of these cells by C. jejuni significantly. Moreover, C. jejuni infection of INT‐407 cells induced tyrosine phosphorylation of several Triton X‐100 soluble proteins with approximate molecular weights of 170, 145, 90, 60 and 55 kDa that were absent or reduced in the presence of genistein in cells after 1 hr of pretreatment. These data suggest that tyrosine protein kinase‐linked pathways strongly regulate the internalization of C. jejuni into intestinal epithelial cells.

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Virulence of Campylobacter species: A molecular genetic approach

Cited by 40 publications

References 121 publications

Different invasion phenotypes of Campylobacter isolates in Caco-2 cell monolayers

Different invasion phenotypes of Campylobacter isolates in Caco-2 cell monolayers

Pathogenesis of Enteric Infection by Campylobacter

Infection with Campylobacter jejuni Induces Tyrosine‐Phosphorylated Proteins into INT‐407 Cells

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