Helicobacter pylori exists in two different morphological forms, spiral and coccoid. This study demonstrated that both forms can infect BALB/c A mice. The animals were inoculated orally three times at 2-day intervals with 10' cfu of both spiral and coccoid forms of strain CCUG 17874 (NCTC 11637), strain 25 and strain 53/93. Infection was followed over a 30-week period by histological scoring of the grade of inflammation in gastric biopsies. At each time point sera were collected for analysis in ELISA and immunoblot analysis. Both spiral and coccoid forms of all H. pylori strains gave significantly higher inflammation scores than a control group of animals 1 week after inoculation. The histological evidence persisted throughout the entire 30 weeks. The inflammation was most severe in the pylorus and duodenum. Infection with strain 553/93 displayed the most severe gastritis. The spiral form of strain CCUG 17874 gave an immune response after only 4 weeks, whereas its coccoid form as well as strains 25 and 5 3 / 9 3 (spiral and coccoid forms) gave a significant increase in antibody response in ELISA and immunoblot after 16 weeks. It is concluded that both spiral and coccoid forms of H. pyluri can cause acute gastritis in BALB/c A mice.

Collagen type-I-binding proteins of Lactobacillus reuteri NCIB 11951 were purified. The cell surface proteins were affinity purified on collagen Sepharose and eluted with an NaCl gradient. Two protein bands were eluted from the column (29 kDa and 31 kDa), and both bound radio-labeled collagen type I. Rabbit antisera raised against the 29 kDa and 31 kDa protein reacted with the affinity-purified proteins in a Western blot with whole-cell extract used as antigen. The N-terminal sequence of the 29-kDa and 31-kDa proteins demonstrated the closest homologies with internal sequences from an Escherichia coli trigger factor protein (TIG.ECOLI). Out of nine other lactobacilli, the antisera reacted only with the L. reuteri and not with the other species tested.

An immunoblot assay for the serological diagnosis of Helicobacter pylori infection was evaluated. Serum samples from patients whose gastric biopsy specimens were known to be positive or negative for H. pylori on culture were used to establish interpretive criteria for the immunoblot assay. A panel of sera from patients with diseases other than H. pylori infection and sera from healthy blood donors were included to validate these criteria. All sera were initially assessed in an enzyme immunoassay (Ge-EIA), based on acid glycine-extracted cell surface proteins of H. pylori NCTC 11637. The same antigen extract was used in the immunoblot assay. In addition, the Ge-EIA and the immunoblot assay were compared with a commercially available EIA (Seradyn, Color Vue Pylori). Bands of 110/120 kDa and/or two of five low-molecular-mass proteins (26, 29, 30, 31, and 33 kDa, in any combination) showed a strong correlation with the H. pylori culture-positive patients (97.5%) compared to the correlation obtained with the EIA results (Ge-EIA, 87.5%; Seradyn EIA, 92.5%), and the antibody responses to these proteins were considered specific reactions. In 37 of 40 serum samples from culture-negative patients and also in sera from patients with other disorders, a moderate antibody reactivity to the medium-size proteins (43 to 66 kDa) was observed, and these were considered not valuable for a specific immunoblot assay. Among sera from culture-positive patients, 39 of 40 serum samples were defined to be immunoblot positive, and from among sera from culture-negative patients, 3 of 40 serum samples were defined to be immunoblot positive. The use of sera from patients with negative cultures for H. pylori as negative controls may decrease the sensitivity due to sampling error and false-negative culture results. Immunoblot assaypositive results were detected among 10% of sera from patients with other diseases, whereas they were detected among 42.5% of sera by the Ge-EIA and 47.5% of sera by the Seradyn-EIA. The higher number of EIA-positive sera in this group reflects a possible cross-reactivity (false-positive EIA result). Of the blood donors, representing asymptomatic but possibly colonized subjects, 24% were immunoblot positive. In conclusion, our data indicate that immunoblotting is more sensitive as well as more specific than EIA. Moreover, it permits detection of antibody responses to specific antigens, e.g., the cytotoxin-associated CagA protein, which may have pathological implications.

An appropriate animal model is essential to study Helicobacter pylori infection. The aim of this study was to investigate if H. pylori can colonise the guinea-pig stomach and whether the infection causes gastritis and a serological response similar to that observed in man. Guinea-pigs were infected either with fresh H. pylori isolates from human gastric biopsies or with a guinea-pig passaged strain. When the animals were killed, 3 and 7 weeks after inoculation, samples were taken for culture, histopathology and serology. H. pylori was cultured from 22 of 29 challenged animals. All culture-positive animals exhibited a specific immune response against H. pylori antigens in Western blotting and gastritis in histopathological examination. Antibody titres in enzyme immunoassay were elevated among animals challenged with H. pylori. The inflammatory response was graded as severe in most animals and consisted of both polymorphonuclear leucocytes and lymphocytes. Erosion of the gastric epithelium was found in infected animals. These results suggest that the guinea-pig is suitable for studying H. pyloriassociated diseases. Moreover, guinea-pigs are probably more similar to man than any other small laboratory animal as regards gastric anatomy and physiology.

The prevalence of H. pylori infection in this periurban community and age group was high. Only serologic methods seem to be unsatisfactory for screening of H. pylori infection in infants and may not reflect the true prevalence. Immunomagnetic separation-PCR is a simple and rapid method for detection of H. pylori in stool and is an attractive method for analysis of colonization in infants. However, it may reflect a different stage of disease than UBT. Further studies are needed to clarify this.