Helical bacteria, like the stomach pathogen H. pylori, swim only about 15% faster than their isogenic rod-shaped mutants.

The swimming strategies of unipolar flagellated bacteria are well known but little is known about how bipolar bacteria swim. Here we examine the motility of Helicobacter suis, a bipolar gastric-ulcer-causing bacterium that infects pigs and humans. Phase-contrast microscopy of unlabeled bacteria reveals flagella bundles in two conformations, extended away from the body (E) or flipped backwards and wrapped (W) around the body. We captured videos of the transition between these two states and observed three different swimming modes in broth: with one bundle rotating wrapped around the body and the other extended (EW), both extended (EE), and both wrapped (WW). Only EW and WW modes were seen in porcine gastric mucin. The EW mode displayed ballistic trajectories while the other two displayed superdiffusive random walk trajectories with slower swimming speeds. Separation into these two categories was also observed by tracking the mean square displacement of thousands of trajectories at lower magnification. Using the Method of Regularized Stokeslets we numerically calculate the swimming dynamics of these three different swimming modes and obtain good qualitative agreement with the measurements, including the decreased speed of the less frequent modes. Our results suggest that the extended bundle dominates the swimming dynamics.

the gastric ulcer and cancer causing bacteria, helicobacter Pylori have uniquely adapted to swim across the viscoelastic mucus gel that lines the stomach epithelial surface and colonize in the harsh acidic environment of the stomach. in this paper we first briefly review results of bacteria tracking and oscillatory shear rheology studies to suggest how the bacteria get across the viscoelastic mucus gel by using a chemical mechanism to raise the pH from acidic to neutral which also triggers a gel to sol transition of mucin. We then present new microrheology studies to show that the bacterium influences the Brownian motion of spherical tracer particles in culture broth solution and in solutions of gastric mucin. the elastic and viscous moduli obtained by tracking particles in the mucin solutions are found to decrease in the presence of bacteria. We also examined the Brownian motion of the bacteria themselves and find that motile bacteria display super-diffusive anomalous Brownian motion while the immotile bacteria exhibit regular diffusive Brownian motion.

We present particle tracking microrheology results on human mucins, isolated from normal surface and gland mucosa and one tumor sample, and examine the motility of Helicobacter pylori in these mucins. At 1.5% concentration human mucin solutions are purely viscous, with viscosity η (gland mucin) > η (surface mucin) > η (tumor mucin). In the presence of motile H. pylori bacteria, particle diffusion is enhanced, with diffusivity D+bac(tumor mucin) > D+bac(gland mucin) > D+bac(surface mucin). The surface and tumor mucin solutions exhibit an elastic response in the presence of bacteria. Taken together these results imply that particle diffusion and active swimming are coupled and impact the rheology of mucin solutions. Both J99 wild type (WT) and its isogenic ΔbabA/ΔsabA mutant swam well in broth or PGM solutions. However, the human mucins affected their motility differently, rendering them immotile in certain instances. The distribution of swimming speeds in human mucin solutions was broader with a large fraction of fast swimmers compared to PGM and broth. The bacteria swam fastest in the tumor mucin solution correlating with it having the lowest viscosity of all mucin solutions. Overall, these results suggest that mucins from different tissue locations and disease status differ in their microrheological properties and their effect on H. pylori motility.

16 To colonize on the gastric epithelium Helicobacter pylori bacteria have to swim across a gradient 17 of pH from 2-7 in the mucus layer. Previous studies of H. pylori motility have shown that at pH 18 below 4 do not swim in porcine gastric mucin (PGM) gels. To separately assess the influence of 19 gelation of PGM and that of pH on motors and pH sensitive receptors of H. pylori, we used 20 phase contrast microscopy to compare the translational and rotational motion of H. pylori in 21 PGM versus Brucella broth (BB10) at different pHs. We observed that decreasing pH leads to 22 decreased fraction of motile swimmers with a decrease in the contribution of fast swimmers to 23 the distributions of swimming speeds and length of trajectories. At all pH's the bacteria swam 24 faster with longer net displacement over the trajectory in BB10 as compared to PGM. While 25 bacteria are stuck in PGM gels at low pH, they swim at low pH in broth, albeit with reduced 26 speed. The body rotation rate and estimated cell body torque are weakly dependent on pH in 27 BB10, whereas in PGM the torque increases with increasing viscosity and bacteria stuck in the 28 low pH gel rotate faster than the motile bacteria. Our results show that H. pylori has optimal 29 swimming under slightly acidic conditions, and exhibits mechanosensing when stuck in low pH 30 mucin gels. INTRODUCTION32 The human stomach presents one of the harshest environments due to the high acidity of its 33 gastric juice secretion and various aspartate proteases and digestive enzymes which are crucial 34 for metabolizing food and destroying microbes. To protect the stomach from its own acidic 35 secretion and control the transport of food, microbes and other ingested products, the epithelial 36 surface of the stomach is lined with a protective, continuous, viscoelastic layer of mucus varying 37 from 100-400 μm in thickness. Across this mucus layer there exists a pH gradient maintained by 38 the co-secretion of bicarbonate [1-3] pH near neutral close to the epithelial surface and highly 39 acidic pH 2-4 on the luminal side during active acid secretion. The pH of the stomach measured 40 at the luminal surface has been shown to range between 0.3 and 2.9 [4,5] with the resting median 41 pH close to 1.74 [5] while the resting pH measured in the mucus layer has been shown to be 42 close to 4 [4]. The mucus derives its viscoelastic properties from the glycoprotein mucin which 43 has been shown to undergo a pH dependent sol to gel transition at pH 4 [6,7] forming a 44 viscoelastic gel below pH 4. Exactly how the gelled mucin prevents the back diffusion of H+ 45 ions is a subject of considerable debate and various processes such as H+ bindng to mucin, 46 Donnan equilibrium, diffusion, viscous fingering have been invoked [8].47 While the combination of gastric juice and the gastric mucus is quite effective in sterilizing and 48 protecting the host from bacteria and infections, the gastrointestinal pathogen, Helicobacter 49 pylori is known to breach this barrier and has adapted to ...