Colonization and tissue tropism of Helicobacter pylori and a novel urease-negative Helicobacter species in ICR mice are independent of route of exposure

Citation
Sn. Mccathey et al., Colonization and tissue tropism of Helicobacter pylori and a novel urease-negative Helicobacter species in ICR mice are independent of route of exposure, HELICOBACT, 4(4), 1999, pp. 249-259
Citations number
47
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
HELICOBACTER
ISSN journal
10834389 → ACNP
Volume
4
Issue
4
Year of publication
1999
Pages
249 - 259
Database
ISI
SICI code
1083-4389(199912)4:4<249:CATTOH>2.0.ZU;2-5
Abstract
Background. In humans, Helicobacter pylori is known to colonize the stomach and to induce persistent gastritis; selected reports also suggest it cause s extragastric disease, including hepatitis. H, pylori and a novel urease-n egative Helicobacter sp, induce gastritis and typhlocolitis, respectively, when inoculated orally into mice. Experimental typhlocolitis and hepatitis have been caused by intraperitoneal (IP) injection of H. hepaticus, H. bili s, and the novel Helicobacter spp. However, the route lay which IF-inoculat ed organisms localize to specific areas of the gastrointestinal system is u nknown. Materials and Methods. To determine whether Helicobacter spp. can be isolat ed from blood, can preferentially colonize specific tissues, and can cause pathological changes, we inoculated 6-week-old outbred mice orally or intra peritoneally with H. pylori or a novel Helicobacter sp. Results. When these mice were inoculated by the IP route, H. pylori was cul tured from lungs, spleen, liver, cecum, and stomach on day 1 after inoculat ion, from liver and stomach mucosa on day 3 after inoculation, and from the stomach on day 30 after inoculation, suggesting preferential colonization of the stomach. After inoculation by the IP route, the novel intestinal Hel icobacter sp, was cultured from the blood, lungs, spleen, liver, kidneys, c ecum, and feces but not from stomach mucosa on day 1 after inoculation. By day 30 after inoculation, the novel Helicobacter sp. was cultured from cecu m and feces only, suggesting that it had preferentially colonized the lower bowel. By the IP route, the novel Helicobacter sp. induced hepatitis that persisted for 30 days after inoculation. Though mice inoculated intraperito neally with H. pylori developed an acute hepatitis, the liver lesion began to resolve 30 days after inoculation. Mice inoculated orally with either H. pylori or the novel Helicobacter sp, did not have hepatitis on day 30 afte r inoculation but developed 100% colonization of stomach and cecum, respect ively. Conclusion. The isolation of H. pylori and the novel Helicobacter sp. from multiple tissues infers that a transient helicobacter bacteremia occurs whe n Helicobacter spy, are injected intraperitoneally, but organisms are clear ed rapidly from nontarget tissues and preferentially colonize specific regi ons of the gastrointestinal tract.