Inability of an isogenic urease-negative mutant stain of Helicobacter mustelae to colonize the ferret stomach

Abstract

Eight ferrets specific-pathogen-free for Helicobacter mustelae were given, per dose, approximately 3.0 ؋ 10 7 CFU of either the wild-type parent strain of H. mustelae (NCTC 12032) (two ferrets), the isogenic ureasenegative mutant strain of H. mustelae (10::Tn3Km) (four ferrets), or sterile culture broth (two ferrets). Infection status was monitored by endoscopic gastric biopsy for urease activity, histopathology, and culture and by serology at 3, 6, 10, and 21 weeks. All ferrets were necropsied at 25 weeks. Both negative control ferrets remained uninfected, both ferrets receiving the H. mustelae wild-type parent strain became infected after two doses of the organism, and all four ferrets given two doses of the isogenic urease-negative mutant strain of H. mustelae remained uninfected throughout the 6-month study. Histopathology correlated with infection status. H. mustelae-infected ferrets exhibited diffuse mononuclear inflammation in the subglandular region and the lamina propria of the gastric mucosa, while uninfected ferrets showed no or minimal inflammation. These results suggest that urease activity is essential for colonization of the ferret stomach by H. mustelae.

Acid resistance of Helicobacter pylori depends on the UreI membrane protein and an inner membrane proton barrier

“…A feature of H. pylori is the constitutive expression of a neutral pH optimum urease at high levels (Mobley et al, 1995). Urease is essential for colonization and for persistence of infection in the stomach (Ferrero et al, 1992;Andrutis et al, 1994;Eaton and Krakowka, 1994;Tsuda et al, 1994). Urease activity maintains a proton motive force (pmf) across the inner cytoplasmic membrane of the bacterium (Meyer-Rosberg et al, 1996;Scott et al, 1998) allowing pmf-driven metabolism even in an acidic environment (Rektorschek et al, 1998).…”

Promotion of Ulcerative Duodenitis in Young Ferrets by Oral Immunization with Helicobacter mustelae and Muramyl Dipeptide

“…elicobacter mustelae shares many of the same biochemical, molecular, and phenotypic characteristics as those found in Helicobacter pylori [1,2]. H. mustelae is a gram-negative, helical, microaerophilic bacterium that adheres tightly to the gastric mucosa and is strongly oxidase-, catalase-, and urease-positive [1].…”

Cell Lysis is Responsible for the Appearance of Extracellular Urease in Helicobacter pylori

“…Urease activity plays an important role in gastric colonization [6]. H. pylori mutants lacking urease are unable to colonize the gastric mucosa of gnotobiotic pigs, mice and ferrets [7][8][9]. Urea hydrolysis by urease produces CO 2 and NH 3 .…”