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