ArticlePLoS pathogens2014
Multivalent adhesion molecule 7 clusters act as signaling platform for host cellular GTPase activation and facilitate epithelial barrier dysfunction.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- The multifunctional type VI secretion system ofApplied and environmental microbiology · 2025Review
- Bacterial adhesion inhibitor prevents infection in a rodent surgical incision model.Virulence · 2020Article
- Review
- Targeting bacterial adherence inhibits multidrug-resistant Pseudomonas aeruginosa infection following burn injury.Scientific reports · 2016Article
- Against the tide: the role of bacterial adhesion in host colonization.Biochemical Society transactions · 2016Review
- Displacement of Pathogens by an Engineered Bacterium Is a Multifactorial Process That Depends on Attachment Competition and Interspecific Antagonism.Infection and immunity · 2016Article
- The expression of heterologous MAM-7 in Lactobacillus rhamnosus reduces its intrinsic capacity to inhibit colonization of pathogen Vibrio parahaemolyticus in vitro.Biological research · 2016Article
- The phospholipid code: a key component of dying cell recognition, tumor progression and host-microbe interactions.Cell death and differentiation · 2015Review
- Biomimetic Materials to Characterize Bacteria-host Interactions.Journal of visualized experiments : JoVE · 2015Article
- Fatal attraction: how bacterial adhesins affect host signaling and what we can learn from them.International journal of molecular sciences · 2015Review
- Dual function of a bacterial protein as an adhesin and extracellular effector of host GTPase signaling.Small GTPases · 2015Article
- Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vibrio parahaemolyticus is an emerging bacterial pathogen which colonizes the gastrointestinal tract and can cause severe enteritis and bacteraemia. During infection, V. parahaemolyticus primarily attaches to the small intestine, where it causes extensive tissue damage and compromises epithelial barrier integrity. We have previously described that Multivalent Adhesion Molecule (MAM) 7 contributes to initial attachment of V. parahaemolyticus to epithelial cells. Here we show that the bacterial adhesin, through multivalent interactions between surface-induced adhesin clusters and phosphatidic acid lipids in the host cell membrane, induces activation of the small GTPase RhoA and actin rearrangements in host cells. In infection studies with V. parahaemolyticus we further demonstrate that adhesin-triggered activation of the ROCK/LIMK signaling axis is sufficient to redistribute tight junction proteins, leading to a loss of epithelial barrier function. Taken together, these findings show an unprecedented mechanism by which an adhesin acts as assembly platform for a host cellular signaling pathway, which ultimately facilitates breaching of the epithelial barrier by a bacterial pathogen.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.