ArticleInfection and immunity2014
Putative Inv is essential for basolateral invasion of Caco-2 cells and acts synergistically with OmpA to affect in vitro and in vivo virulence of Cronobacter sakazakii ATCC 29544.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 27 citations in OpenAlex.
- DecipheringMicroorganisms · 2026Review
- Probiotic Saccharomyces boulardii Against Cronobacter sakazakii Infection: In Vitro and In Vivo Studies.Probiotics and antimicrobial proteins · 2026Article
- Indispensable role of AcrEF in modulating Salmonella virulence and disrupting host tight junctions to facilitate paracellular entry and invasion.Biology direct · 2025Article
- Characterization of Molecular Chaperone GroEL as a Potential Virulence Factor inFoods (Basel, Switzerland) · 2023Article
- Effects ofFoods (Basel, Switzerland) · 2023Article
- Profiling the Virulence and Antibiotic Resistance Genes ofFrontiers in microbiology · 2021Article
- Deletion of theGut microbes · 2020Article
- Genomic Analysis of Putative Virulence Factors Affecting Cytotoxicity ofFrontiers in microbiology · 2019Article
- New virulence factor CSK29544_02616 as LpxA binding partner in Cronobacter sakazakii.Scientific reports · 2018Article
- A Cronobacter turicensis O1 antigen-specific monoclonal antibody inhibits bacterial motility and entry into epithelial cells.Infection and immunity · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cronobacter sakazakii is an opportunistic pathogen that causes neonatal meningitis and necrotizing enterocolitis. Its interaction with intestinal epithelium is important in the pathogenesis of enteric infections. In this study, we investigated the involvement of the inv gene in the virulence of C. sakazakii ATCC 29544 in vitro and in vivo. Sequence analysis of C. sakazakii ATCC 29544 inv revealed that it is different from other C. sakazakii isolates. In various cell culture models, an Δinv deletion mutant showed significantly lowered invasion efficiency, which was restored upon genetic complementation. Studying invasion potentials using tight-junction-disrupted Caco-2 cells suggested that the inv gene product mediates basolateral invasion of C. sakazakii ATCC 29544. In addition, comparison of invasion potentials of double mutant (ΔompA Δinv) and single mutants (ΔompA and Δinv) provided evidence for an additive effect of the two putative outer membrane proteins. Finally, the importance of inv and the additive effect of putative Inv and OmpA were also proven in an in vivo rat pup model. This report is the first to demonstrate two proteins working synergistically in vitro, as well as in vivo in C. sakazakii pathogenesis.
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