Cheryl Neace

Prevalence of CagA, VacA antibodies in symptomatic and asymptomatic children with Helicobacter pylori infection.

Background. Limited data are available on the prevalence of CagA and VacA Helicobacter pylori antibodies in children. The aim of this study was to investigate the antibody prevalence to the H. pylori virulence factors CagA and VacA in symptomatic and asymptomatic children with H. pylori infection and to correlate these antibodies with the severity of gastric inflammation or density of H. pylori organisms in the gastric mucosa.

Comparison between a rapid office-based and ELISA serologic test in screening for Helicobacter pylori in children.

The rapid diagnostic serological test for detection of Helicobacter pylori (H. pylori) infection in children has a significant advantage over the standard enzyme immunoassay (EIA) method, for its simplicity and rapid availability of results in a physician’s office setting. We compared the immunochromatographic test with a standard enzyme immunoassay test in the pediatric population.

Is Sudden Infant Death Syndrome Associated with Helicobacter pylori Infection in Children

Helicobacter pylori infection has recently been implicated in the pathogenesis of sudden infant death syndrome (SIDS). We investigated this association. Twenty‐five pairs of gastric and tracheal tissue specimens obtained from autopsies of 25 children with previous diagnoses of SIDS were available for this study. The presence of H. pylori organisms was evaluated by three different methods: histology (hematoxylin‐eosin or Giemsa staining), immunohistochemistry, and nested polymerase chain reaction technique. We were unable to confirm the presence of H. pylori organisms by the first two methods. H. pylori DNA was identified by nested polymerase chain reaction in six different tissue specimens (stomach, 4; trachea, 2). In no case was H. pylori DNA detected in both tissues. We concluded that H. pylori infection is most likely not associated with SIDS.

Detection of Helicobacter pylori organisms by Hp-fast in children.

Hp-fast is a new rapid urease test (RUT) thathas not been evaluated in children. The aim of the studywas to prospectively compare the Hp-fast test to theCLOtest in children. Children with gastrointestinal symptoms who undergo diagnostic upper endoscopywere prospectively enrolled to the study. Antral gastricbiopsies were evaluated for histology and for CLO-testand Hp-fast. Results were then compared to histology. Of the 94 children who participated,gastritis was found in 38 (40%), of whom 16 (42%) hadassociated H. pylori organisms. In two children, H.pylori organisms were identified without gastritis. The concordance between both RUT tests was 98%.A significant correlation was found between RUT resultsand histological factors or serology. The accuracy rateof both RUT increased significantly when different gold standards were utilized todetect Hp infection in children. The best correlationwas found when histology and serology were considered asthe gold standard for the diagnosis of H. pylori infection in children (sensitivity: 100%compared to 43-80% with other standards, respectively).In conclusion, the Hp-fast test result is comparable toCLOtest, but neither alone is sufficient to establish the diagnosis of Hp infection inchildren.

Vitamin A and retinoic acids immunomodulation on human gut lymphocytes.

Epidemiological studies have suggested an important immunomodulatory role for vitamin A and other related vitamin A compounds in adults and children. Although vitamin A is absorbed via the gastrointestinal tract, its affect on the gut mucosal immune cells has not been adequately investigated. We investigated the in-vitro effect of vitamin A (retinol) and its retinoid acid (RA) compounds (13-cis- and all trans-retinoic acids) on the human gut mucosal immune system as represented by colonic lamina propria lymphocyte (LPL) proliferation, and ornithine decarboxylase (ODC) activity. Results showed that retinol suppressed and trans-retinoic acid enhanced thymidine incorporation into LPL. 13-cis retinoic acid did not significantly affect LPL DNA synthesis. Similarly, retinol (0.025 microgram/ml and 10 micrograms/ml) and 13-cis retinoic acid (conc. 10 micrograms/m) suppressed, while all trans-retinoic acid (conc. 10 micrograms/ml) enhanced ODC activity in PHA-stimulated LPL. Interestingly, the effects of retinol and all trans-RA were abolished when LPL were previously depleted of macrophages. Addition of monocyte-associated lymphokines, IL-1 and IL-6, showed that IL-1 partially replaced the enhancing effect of all trans-RA previously observed on LPL thymidine incorporation. IL-6 did not affect LPL DNA synthesis irrespective of the vitamin A compound used. We conclude that retinol and retinoid acids (13-cis, all trans-) may alter the human colonic immune system possibly via IL-1 cytokine, but not via IL-6. The data suggest that vitamin A and its retinoid compounds may participate in the modulation of the gut immune system.

Immunosuppressive effect of budesonide on human lamina propria lymphocytes

Budesonide, a beta-adreno-receptor agonist, is comparable to corticosteroid in the treatment of patients with inflammatory bowel disease with the advantage of minimal side effect. Although the immunomodulatory effects of budesonide on the circulatory and respiratory mucosal immune system have been reported, its effect on the human gut immune system has not been published. In this study, the effect of budesonide on the human gut immune system was compared to methyl-prednisolone. The cellular immune function was measured in-vitro by DNA synthesis, ornithine decarboxylase (ODC) activity and TNFalpha secretion. We found that both drugs have a comparable inhibitory effect on DNA synthesis, ODC activity and suppression of TNFalpha secretion. Exogenous addition of IL-2, did not restore the antiproliferative effect of both drugs. We conclude that budesonide has a comparative suppressive effect to methyl-prednisolone on the gut immune system which is not related to IL-2 secretion. The antiproliferative response may explain the therapeutic effect of budesonide on patients with inflammatory bowel disease.

TYROSINE KINASE AND ORNITHINE DECARBOXYLASE ACTIVATION IN CHILDREN WITH HELICOBACTER PYLORI GASTRITIS

H. pylori infection has been considered a risk factor for the development of gastric malignancy. Ornithine decarboxylase and tyrosine kinases activities are increased in patients with colon or esophageal cancer. In this study we compared the ODC and tyrosine kinases activities in the gastric mucosa of children with H. pylori infection and normal mucosa. Gastric biopsies were prospectively collected from children during routine upper endoscopic procedure. H. pylori infection was determined histologically. Biopsies were analyzed for ODC activity, total tyrosine kinases activities, and for the activity of protooncogene tyrosine kinase pp60c-src. The mean ODC activity (pmol14CO2/mg. protein/hr) and total tyrosine kinases activity (pmol32P/mg. protein) were 186 and 5877 for H. pylori infected mucosa; and 229 and 4300, for normal mucosa, respectively (p > 0.05). Tyrosine kinase pp60c-src protein levels were similar between H. pylori infected mucosa and normal mucosa (3.12 and 2.15 pmol32P/mg. protein, respectively; p > 0.05). There was no correlation between gastric inflammation and the level of ODC or tyrosine kinase activities. ODC and tyrosine kinase activities in the gastric mucosa are similar in children with H. pylori infection compared to normal mucosa. The data suggest that these enzymes cannot be used as markers for future cancer development in children.

H. Pylori Strains in Symptomatic and Asymptomatic Children From WV 576

H. pylori (HP) strains, Cag-A/Vac-A, determine the bacterial virulence and affect the morbidity and mortality. The prevalence of these strains in the pediatric population in the US is unknown.

THE IMMUNOMODULATORY EFFECT OF BUDESONIDE (BD) AND METHYLPREDNISOLONE(MP) ON THE HUMAN GUT IMMUNE SYSTEM † 693

THE IMMUNOMODULATORY EFFECT OF BUDESONIDE (BD) AND METHYLPREDNISOLONE(MP) ON THE HUMAN GUT IMMUNE SYSTEM † 693