Expression of mature IL-18 and CASPase-1 in Helicobacter pylori infected gastric mucosa

Abstract

wild cheetahs without gastritis. The purpose of this work was to identify the Helicobacter species associated with gastritis in captive cheetahs and those that were apparently commensal in wild cheetahs. Methods: 16S rDNA was amplified with universal eubacterial primers from gastric tissue samples from 5 wild and 5 captive cheetahs. Overlapping PCR products that included nearly the entire 16S rRNA gene were sequenced on both strands. Morphological characteristics were determined by light and transmission electron microscopy. To further characterize the species of the Helicobacter-like organisms, portions of the urease gene were amplified using primer pairs homologous to urease from H. heilmannii but different from H. pylori. Results: Light and electron microscopy in all captive and wild cheetahs revealed tightly coiled spiral organisms with a morphology that was indistinguishable from H. heilmannii . No H. pylori-like bacteria were seen. Surprisingly, eight cheetahs (5 wild, 3 captive) were infected with Helicobacter whose 16S rDNA sequences were 99% similar to that of H. pylori, and only 95% similar to H. acinonychis, the Helicobacter previously identified in cheetahs. Amplification of urease with primers specific for H. heilmannii did not yield product in any of these animals, which is consistent (though not definitive) with their identification as H. pylori-like. Two captive cheetahs harbored Helicobacter with 16S rDNA that was 97% similar to what has been called H. heilmannii 2, which is part of the H. felis species group. Urease amplification with H. heilmannii primers from one of these animals for which material was available revealed appropriate sized bands, consistent with the 16S rDNA sequence. Conclusions: Captive and wild cheetahs are commonly infected with an H. pylori-like organism that resembles H. heilmannii morphologically. The presence of similar bacteria in cheetahs with and without disease suggests that the immune response, rather than infection alone, is responsible for the gastritis.