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Fig. 1 | Gut Pathogens

Fig. 1

From: Outer membrane phospholipase A’s roles in Helicobacter pylori acid adaptation

Fig. 1

H. pylori acid adaptation model. This figure schematically depicts our hypothesis on how H. pylori uses urea in acid protection. A Urea passes through OMPLA into the periplasm simply driven by the diffusion gradient. B Urea then diffuses through the proton-dependent inner membrane (IM) urea channel UreI to the cytoplasm. C Urease converts urea into NH3 and CO2. D These molecules diffuse into the periplasm. CO2 diffuses through the membrane simply following the gradient. At pH around 6 NH3 will largely be converted to NH4 + that passes through IM channels. A very small portion of NH3 will continuously remain and a small fraction of this NH3 will diffuse through the IM. E Most of the CO2 diffuses out of the cell, but some is converted by the periplasmic enzyme α-carbonic anhydrase (αCA) into bicarbonate. This bicarbonate forms a buffer that helps maintaining the periplasmic pH around 6.1. A sudden enlarged influx of protons will be buffered by this bicarbonate. F NH4 + leaves the cell mainly through OMPLA. The toxicity sign represents the damage caused by NH4 + in the gastric mucosa. The pH gradient is indicated in the colour bar at the right-hand side. PDB files used in this illustration: 3UX4 [15] (UreI; blue), 4XFW [16] (αCA; orange) and 1E9Y [17] (Urease; grey). The red structure shown twice in the outer membrane, is a homology model (H. pylori OMPLA model based on the 1QD5 [14] PDB template). The purple and turquoise proteins embedded in the right-front corner of the IM are COG0733 transporter models. We suggest these transporters can diffuse NH4 + (and NH3?) across the IM (we call them ammonium channels I and II, AmCI and AmCII; these models are based on the 4US3 [18] PDB template structure). This figure does not reflect real-life concentrations

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