Kenjiro Konno

HYPERPLASIA OF GASTRIC MUCOSA IN DONOR RATS ORALLY INFECTED WITH TAENIA TAENIAEFORMIS EGGS AND IN RECIPIENT RATS SURGICALLY IMPLANTED WITH THE LARVAE IN THE ABDOMINAL CAVITY

Abstract Rats heavily infected with Taenia taeniaeformis larvae in the liver show a remarkable increase in their stomach weight, hyperplasia, and hypergastrinemia. However, it is unknown what causes these phenomena. Hence, as a preliminary study to investigate the importance of larval parasitism in the liver, two experiments were done. In the first experiment, 14 donor rats were orally inoculated with 3,000 T. taeniaeformis eggs. In the second experiment, 136–300 of the larvae obtained from the rats were surgically implanted into the abdominal cavity of 7 recipient rats. Gastrin levels and histopathological changes in the gastric mucosa were investigated. In all, 11 donor rats showed hypergastrinemia and hyperplasia, 5 recipient rats showed gastric mucosal hyperplasia accompanied by excessive mucous cell proliferation, and 2 recipient rats showed hypergastrinemia. These results suggest that parasitism of the liver by the larvae is not essential for the development of hyperplasia and that factors from the larvae might cause these phenomena.

Concomitant onset of hypergastrinemia, intragastric alkalinity and gastric hyperplasia, and numbers of antral G cells in Taenia taeniaeformis-infected rats

Abstract Infection of hepatic larvae of Taenia taeniaeformis is associated with gastropathy in rats. The sequence of occurrence of the prominent changes, i.e. gastric hyperplasia, intragastric alkalinity and hypergastrinemia, could provide an insight on the pathogenetic mechanism(s) involved in the induction of gastric changes. Density of gastrin producing antral G cells was also examined to determine the cause of hypergastrinemia. Five-week-old, male Wistar rats were orally infected with approximately 4000 Taenia taeniaeformis eggs and examined for changes of stomach morphology, intragastric pH, and serum gastrin every 2 weeks post-infection. Numbers of antral G cells were determined by quantitative immunohistochemistry. Gastric hyperplasia, hypergastrinemia, and rise of intragastric pH occurred concomitantly 56 days post-infection. Mean number of G cells per 100 μm2 antral mucosa in infected rats was comparable to uninfected controls, although there was an apparent increase in width of antral mucosal sections in hyperplastic stomachs. The concomitant onset of gastric hyperplasia, intragastric alkalinity and hypergastrinemia, most likely indicate that chemical mediators are involved which primarily mediate rapid hyperplasia of mucus-secreting cells. Hypergastrinemia associated with this condition could be due to antral G-cell hyperfunction. However, an increase in total antral G-cell population should be considered because of gross enlargement of hyperplastic stomachs.

Gastric hyperplasia and parietal cell loss in Taenia taeniaeformis inoculated immunodeficient mice.

Immunodeficient mice were studied to determine their suitability as models in investigating the role of Taenia taeniaeformis larval products in the development of gastric hyperplasia. Recombinant active gene 2 (RAG2)-deficient and severe combined immune-deficient (SCID) mice were studied as candidate animal models. RAG2-deficient mice inoculated orally with T. taeniaeformis eggs developed gastric hyperplasia with alcian blue-periodic acid-Schiff-positive cell proliferation similar to those of rats. SCID mice inoculated with different doses and routes of T. taeniaeformis in vitro-hatched oncospheres and those orally inoculated with eggs resulted also in different degrees of gastric hyperplasia. Influence of inoculation forms of parasite, doses and routes of inoculation on initiation of hyperplastic gastropathy was suggested to be dependent on number and size of developed larvae. Both RAG2-deficient and SCID mice with hyperplastic mucosa were observed with significant loss of parietal cells. Apparent decrease in parietal cell number was observed in SCID mice at 2 weeks after intraperitoneal inoculation with oncospheres before hyperplastic lesions developed. Earliest occurrence of gastric hyperplasia in SCID mice was observed at 3 weeks after oral inoculation of in vitro-hatched oncospheres, sooner than orally inoculated rats. The results suggested that these immunodeficient mice could be used as animal models to study factors involved in T. taeniaeformis-induced gastric mucous cell hyperplasia.