Emily Goers Sweeney

TL;DR: It is proposed that H. pylori has evolved a sensitive urea chemodetection and destruction system that allows the bacterium to dynamically and locally modify the host environment to locate the epithelium.

TL;DR: It is concluded that H. pylori perceives LuxS-produced AI-2 as a chemorepellent via the chemoreceptor TlpB, supporting the model that tlpB functions in a signalling pathway downstream of luxS and upstream of cheA, which is non-responsive to a gradient or uniform distribution of the chemical.

TL;DR: It is shown that urea and the urea-binding site residues play critical roles in the ability of H. pylori to sense acid and the signaling model predicts that protonation events at Asp114, affected by changes in pH, dictate the stability of TlpB through urea binding.

TL;DR: This study studied how chemorepulsion of Helicobacter pylori from the universal quorum signal autoinducer-2 (AI-2) shapes the spatial organization of its biofilms and concluded that chemotaxis from AI-2 is a determinant of H.pylori biofilm spatial organization and dispersal.

TL;DR: These findings indicate that H. pylori has evolved at least two independent receptors capable of detecting acid gradients, allowing not only survival in the stomach, but also controlling the interaction of the bacteria with the epithelium.