Infection with <i>Campylobacter jejuni</i> Induces Tyrosine‐Phosphorylated Proteins into INT‐407 Cells

Biswas, Debabrata; Niwa, Hidekazu; Itoh, Kazuyoshi

doi:10.1111/j.1348-0421.2004.tb03509.x

Cited by 21 publications

(15 citation statements)

References 33 publications

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“…If non-culturable C. jejuni can adhere or invade but cannot recover their culturability, measuring the adhesion and invasion would result in an underestimation of the infectivity, although the curves in the Figure would be affected. The curves all show an increase in the number of bacteria adhering to and/or invading INT-407 cells/well until a maximal is reached, as previously described by Biswas and colleagues [21,32,33]. If non-culturable C. jejuni were able to adhere or invade, but not to recover their culturability, a competition with the culturable C. jejuni would be expected.…”

Section: Discussionsupporting

confidence: 68%

Lack of response of INT-407 cells to the presence of non-culturableCampylobacter jejuni

2007

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SUMMARYMany contradictory articles on the infectivity of non-culturable Campylobacter jejuni can be found. We studied the effect of non-culturable C. jejuni in an in vitro assay. To prevent the potential effect of a few culturable bacteria in the non-culturable suspension, INT-407 cells, which mimic the outer cell layer in the small intestines, were exposed to culturable C. jejuni suspensions with or without non-culturable C. jejuni. The number of bacteria adhering to and/or invading INT-407 cells and the IL-8 secretion were measured. No differences were found between bacterial suspensions with or without non-culturable C. jejuni added. These findings show that non-culturable C. jejuni do not adhere to or invade INT-407 cells and do not induce an immune response. As previous studies showed a correlation between the used in vitro assays and the effect in vivo, our study strongly suggests that culturability is a good indicator of the risk for C. jejuni infection.

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Section: Discussionsupporting

confidence: 68%

Lack of response of INT-407 cells to the presence of non-culturableCampylobacter jejuni

2007

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“…jejuni is capable of invading gut tissue cells [9-11]. In general, bacterial entry into host cells in vitro may proceed by microtubule-dependent and/or actin-dependent pathways [10,12,13]. C. jejuni encodes numerous outer-membrane proteins with proposed roles in bacterial adhesion such as CadF, FlpA, JlpA and PEB1 [14-17].…”

Section: Introductionmentioning

confidence: 99%

The signaling pathway of Campylobacter jejuni-induced Cdc42 activation: Role of fibronectin, integrin beta1, tyrosine kinases and guanine exchange factor Vav2

et al. 2011

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BackgroundHost cell invasion by the foodborne pathogen Campylobacter jejuni is considered as one of the primary reasons of gut tissue damage, however, mechanisms and key factors involved in this process are widely unclear. It was reported that small Rho GTPases, including Cdc42, are activated and play a role during invasion, but the involved signaling cascades remained unknown. Here we utilised knockout cell lines derived from fibronectin-/-, integrin-beta1-/-, focal adhesion kinase (FAK)-/- and Src/Yes/Fyn-/- deficient mice, and wild-type control cells, to investigate C. jejuni-induced mechanisms leading to Cdc42 activation and bacterial uptake.ResultsUsing high-resolution scanning electron microscopy, GTPase pulldowns, G-Lisa and gentamicin protection assays we found that each studied host factor is necessary for induction of Cdc42-GTP and efficient invasion. Interestingly, filopodia formation and associated membrane dynamics linked to invasion were only seen during infection of wild-type but not in knockout cells. Infection of cells stably expressing integrin-beta1 variants with well-known defects in fibronectin fibril formation or FAK signaling also exhibited severe deficiencies in Cdc42 activation and bacterial invasion. We further demonstrated that infection of wild-type cells induces increasing amounts of phosphorylated FAK and growth factor receptors (EGFR and PDGFR) during the course of infection, correlating with accumulating Cdc42-GTP levels and C. jejuni invasion over time. In studies using pharmacological inhibitors, silencing RNA (siRNA) and dominant-negative expression constructs, EGFR, PDGFR and PI3-kinase appeared to represent other crucial components upstream of Cdc42 and invasion. siRNA and the use of Vav1/2-/- knockout cells further showed that the guanine exchange factor Vav2 is required for Cdc42 activation and maximal bacterial invasion. Overexpression of certain mutant constructs indicated that Vav2 is a linker molecule between Cdc42 and activated EGFR/PDGFR/PI3-kinase. Using C. jejuni mutant strains we further demonstrated that the fibronectin-binding protein CadF and intact flagella are involved in Cdc42-GTP induction, indicating that the bacteria may directly target the fibronectin/integrin complex for inducing signaling leading to its host cell entry.ConclusionCollectively, our findings led us propose that C. jejuni infection triggers a novel fibronectin→integrin-beta1→FAK/Src→EGFR/PDGFR→PI3-kinase→Vav2 signaling cascade, which plays a crucial role for Cdc42 GTPase activity associated with filopodia formation and enhances bacterial invasion.

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“…The pathophysiology of diarrheal disease caused by C. jejuni is poorly defined [1,21,22]. Studies of Campylobacter enteritis in sporadic cases and outbreaks indicate that milk, water and poultry meat are major environmental sources [20].…”

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confidence: 99%

Age-Dependent Variation of Virulence-Associated Genes Retained in Campylobacter jejuni Isolated from Chickens in a Poultry Farm

2009

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ABSTRACT. The presence of 11 virulence-associated genes in Campylobacter jejuni isolated from chickens at different stages of their development was examined by PCR. Multiple groups of C. jejuni were colonized in one chicken at the same time. Two hundred thirty one C. jejuni in total were isolated from the same group at four different ages and 12 groups of C. jejuni possessing of 11 virilence-associated genes were observed. Eleven, eight, five and three groups of C. jejuni were detected at 21, 28, 42 and 56 days after hatching, respectively. The variation of Campylobacter groups was reduced as the chicken developed and one group of C. jejuni became predominant.

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

Cited by 21 publications

References 33 publications

Lack of response of INT-407 cells to the presence of non-culturableCampylobacter jejuni

Lack of response of INT-407 cells to the presence of non-culturableCampylobacter jejuni

The signaling pathway of Campylobacter jejuni-induced Cdc42 activation: Role of fibronectin, integrin beta1, tyrosine kinases and guanine exchange factor Vav2

Age-Dependent Variation of Virulence-Associated Genes Retained in Campylobacter jejuni Isolated from Chickens in a Poultry Farm

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