Figure 6.

Gastric acid secretion by human gastric mucosal biopsies is inhibited by wild-type H pylori strains. Gastric biopsies were infected with wild-type H pylori strain 60190, P12 or P12 ΔcagL (1—2×10⁵ bacteria/mg wet weight biopsy, 15 h) or Brucella broth alone, and then incubated with 150 μM 5-(N-ethyl-n-isopropyl) amiloride (EIPA) with or without 50 μM SCH28080 for 30 min. The pH of the medium bathing the biopsies was measured continuously for 3 min at 7 min intervals. After 21 min, histamine (or vehicle) was added to some biopsies to a 1 mM final concentration (arrows). (A) Changes in extracellular pH of three representative biopsies are shown as a function of time. Open squares, biopsy treated with vehicle alone; open triangles, biopsy treated with histamine; and open circles, biopsy infected with wt H pylori strain 60190 and treated with histamine. (B) The slopes of the initial rates of change of extracellular pH of medium bathing the biopsies as shown in A were transformed for buffer capacity to yield the biopsy proton production rate (PPR; pmol H⁺/min). Open squares, biopsies treated with vehicle alone; open triangles, biopsies treated with histamine; and open circles, biopsies infected with wild-type H pylori strain 60190 and treated with histamine. (C) Open triangles, biopsy treated with histamine in the absence of SCH28080; open diamonds, biopsy treated with 50 μM SCH28080 for 30 min and then treated with histamine. (D) Open triangles, biopsy treated with histamine; open diamonds, biopsy infected with wild-type H pylori strain P12; asterisks, biopsy infected with the H pylori P12 ΔcagL isogenic mutant. Data points in (B) and (C) are the mean PPR ±SD, n=3 biopsies; data points in (D) are measurements of single biopsies.