Helicobacter pylori moves through mucus by reducing mucin viscoelasticity
by Celli, J.P., Turner, B.S., Afdahl, N.H., Keates, S., Ghiran, I., Kelly, C., Ewoldt, R.H., McKinley, G.H., So, P., Erramilli, S. and Bansil, R.
The ulcer-causing gastric pathogen Helicobacter pylori, is the only bacterium known to
colonize the harsh acidic environment of the human stomach. It is well established that H. pylori
accomplishes this by production of the enzyme urease, which catalyzes hydrolysis of urea to
yield ammonia thus elevating the pH of its environment. However, the manner in which H. pylori
is able to swim through the viscoelastic mucus gel that coats the stomach wall remains poorly
understood. Previous rheology studies on gastric mucin, the key viscoelastic component of
gastric mucus, indicate that the rheology of this material is profoundly pH dependent,
transitioning from a viscous solution at neutral pH to a gel in acidic conditions. Bulk rheology
measurements on porcine gastric mucin (PGM) show that pH elevation by H. pylori in the
presence of urea induces a dramatic decrease in the viscosity and elastic modulus. Microscopy
studies of the motility of H. pylori in gastric mucin at acidic and neutral pH in the absence of
urea show that the bacteria swim freely at high pH, and are strongly constrained at low pH.
Using two-photon fluorescence microscopy to image the bacterial motility in an initially low pH
mucin gel with urea present we show that the gain of translational motility by bacteria is directly
correlated with a rise in pH indicated by BCECF, a pH sensitive fluorescent dye. Our study
shows that the common perception of the helical bacterium moving in a corkscrew like manner
through a viscoelastic gel is wrong.