Intraluminal casein model of necrotizing enterocolitis for assessment of mucosal destruction, bacterial translocation, and the effects of allopurinol and N-acetylcysteine.

An intraluminal casein model (ICM) of necrotizing enterocolitis (NEC) is able to produce small-bowel changes reminiscent of human NEC in neonatal animals. We studied bacterial translocation (BT) in NEC induced by using the ICM in neonatal piglets. We also studied whether allopurinol (AL) and N-acetylcysteine (NAC) have an effect on BT and mucosal changes in the ICM of NEC. Twenty-eight neonatal piglets were randomized into four groups. NEC was induced in 21 by injecting casein-d-gluconate into a loop of terminal ileum: group Cas (n = 7) had no premedication, in group Cas/AL (n = 7) intravenous (i.v.) Al (100 mg/kg), and in group Cas/NAC (n = 7) i.v. NAC (200 mg/kg) was given. Group Sham (n = 7) had the ileum injected with 0.9% saline with no premedication. Immediately after the injection a mesenteric lymph node (MLN) adjacent to the loop was harvested for quantitative aerobic bacterial culture; 4 h after the injection another MLN and samples of spleen, liver, kidney, and lung were harvested and cultured. Comparison of the incidence of samples with positive bacterial cultures and the number of colony-forming units (CFU) in samples was made between groups. The severity of NEC in the ileum was graded from 0 to 3 according to macroscopic and histologic findings. NEC changes in the bowel were most severe in Cas piglets, less severe in Cas/NAC piglets ( P < 0.5), and sham piglets had the least severe changes ( P < 0.05). piglets with NEC changes in the ileum had a higher incidence of BT into the MLN than piglets without NEC changes ( P < 0.05), but the difference in CFU was not significant ( P > 0.05). In Cas and Cas/NAC piglets a high incidence of BT into the MLN was noted as early at -5 min after casein injection. The incidence of BT into the MLN was significantly higher in Cas and Cas/NAC piglets than in Sham piglets ( P < 0.05), the difference in CFU being not significant ( P > 0.05). BT in Cas/Al piglets was not significantly different from that of Cas piglets ( P > 0.05), but less than in Cas/NAC piglets ( P < 0.05). Four hours after casein injection into the ileum there was significant BT into the MLN. Premedication with NAC was associated with less severe NEC changes, but neither NAC nor AL significantly affected BT.

Parietal cell antibodies and Helicobacter pylori in children.

BACKGROUND: Gastric autoantibodies are common in Helicobacter pylori-infected adults, and the presence of these antibodies is associated with atrophic gastritis. The role of H. pylori in the autoimmune type of atrophic gastritis is unresolved, and it is not known at what stage the autoantibodies appear in serum during H. pylori infection. Therefore, we screened children with and without H. pylori infection for gastric parietal cell antibodies. METHODS: Seventy-one children with H. pylori infection verified by examination of gastric biopsy specimens (mean age, 9.4 years), 8 children with positive serology but negative histology for H. pylori (mean age, 11.6 years), and 130 children with negative serology for H. pylori (mean age, 7.7 years) were screened for the presence of gastric parietal cell antibodies in serum by indirect immunofluorescence. In addition, 61 children with celiac disease (mean age, 7.1 years) were screened for gastric parietal cell antibodies and H. pylori antibodies. RESULTS: None of the children with H. pylori infection had gastric parietal cell antibodies in serum. Only three positive parietal cell antibody reactions were found: a 14-year-old boy with positive serology for H. pylori but no other signs of infection (titer 5000), a 14-year-old girl with tuberculosis (titer 1250, seronegative for H. pylori) and a 10-year-old girl with insulin-dependent diabetes mellitus (titer 6250, seronegative for H. pylori). CONCLUSIONS: Although gastric autoantibodies are often found in adults with chronic H. pylori gastritis, it seems that H. pylori-infected children are not positive for gastric parietal cell antibodies. It remains to be studied in which H. pylori infections and at what stages gastric autoantibodies appear.

Identification of hippurate-negative thermophilic campylobacters.

Twenty-eight thermophilic campylobacter isolates showing negative hippurate hydrolysis were further characterized. Using Campylobacter jejuni and coli specific primers for ceuE gene, five of the isolates with repeatedly negative results in rapid hippurate hydrolysis were positive in C. jejuni-specific polymerase chain reaction (PCR) and 13 isolates were shown to be C. coli. All except one isolate with positive results in C. jejuni PCR were negative in C. coli PCR including those with repeatedly negative hippurate hydrolysis results. One isolate was positive in both PCRs due to a mixed culture. In comparison with PCR, API Campy gave concordant results in only 20 of the 28 isolates tested. Hybridization with PCR probes for ceuE gene of known C. jejuni and coli strains confirmed PCR results in all 27 isolates tested. In contrast to hippurate hydrolysis, PCR seemed to be a more reliable method to identify C. coli.

Helicobacter antibodies in Finnish centenarians.

BACKGROUND: The prevalence of helicobacter antibodies increases with age and, in many developed countries, is highest in people born before 1940. Data on very old subjects are, however, limited. In this study we wanted to determine whether the age-related increase in the seroprevalence of H. pylori infection continues even in the oldest age group alive in Finland, the centenarians. METHODS: Sera from 173 subjects (93% of all centenarians alive in Finland in 1991) were available for the present study. IgG and IgA antibodies against H. pylori were determined by an in-house enzyme immunoassay. To estimate the influence of atrophic gastritis on the prevalence of helicobacter antibodies, serum pepsinogen I (PG I) concentrations and parietal cell antibodies (PCAs) were measured by an enzyme immunoassay and indirect immunofluorescence, respectively. RESULTS: The prevalence of helicobacter antibodies in Finnish centenarians was 66%. Low PG I values (<28 microg/l) were found in 36% and positive PCAs in 16% of the subjects studied. The prevalence of PCAs was especially high (50%) in H. pylori-negative subjects with low PG I values, suggesting severe gastric atrophy. CONCLUSIONS: The age-related increase in H. pylori seroprevalence did not continue in the oldest age group alive in Finland. This may be explained partly by a relatively high frequency of atrophic gastritis (as suggested by low PG I values) in H. pylori-negative centenarians, but other factors--such as selective H. pylori-related mortality--may also have contributed to the fairly low seroprevalence (66%) observed.