Figure 2.

 Histology of the gastric pyloric mucosa of (A) control, (B) wild-type Helicobacter pylori strain TN2GF4, (C) its isogenic cagG knockout mutant, or (D) virD4 knockout mutant. Haematoxylin and eosin stain, original magnification ×200. (A) In controls, inflammatory cell infiltration in the lamina propria was negligible throughout the experimental periods. (B) In gerbils infected with the wild-type strain, pyloric mucosa showed marked infiltration by neutrophilic polymorphonuclear cells and mononuclear cells at four weeks after inoculation and the inflammatory response increased with the duration of infection. The pyloric mucosa became thickened from four weeks after inoculation, and irregularly branched and dilated mucous glands appeared at 24 weeks after inoculation. (C) In gastric mucosa infected with the cagG knockout mutants, inflammatory cell infiltration in the lamina propria was negligible throughout the experimental periods. (D) Pyloric mucosa of gerbils infected with the virD4 knockout mutants showed mild inflammatory inflammation at four and 12 weeks after inoculation. At 24 weeks after inoculation, pyloric mucosa showed increased degrees of inflammatory cell infiltration and became thickened.