Household and socioeconomic characteristics were obtained by interviews. Results:  The prevalence of H. pylori infection increased from 49.7% (95% CI 42.8, 56.7) in 2004 to 58.9% (95% CI 51.8, 65.6) in 2007–2009. Among children tested in both

examinations, 69 (49.3%) had persistent infection, 14 (10.0%) IDO inhibitor were new cases, 56 (40.0%) remained uninfected, and one (0.7%) had lost H. pylori infection. The approximate annual incidence of infection during 2004–2009 was 5%. Sibling’s H. pylori positivity at baseline increased the risk for late acquisition of H. pylori infection; adjusted prevalence ratio (PR) 4.62 (95% CI 0.76, 28.23) (p = .09), while maternal education lowered the risk; adjusted PR 0.84 (95% CI 0.69, 1.01) (p = .06). Sibling’s H. pylori positivity was the only significant variable associated with early and persistent H. pylori infection in multivariate analysis. Conclusions:  Most H. pylori infections are acquired at preschool age and transient infection beyond this age is uncommon in this population. Helicobacter pylori-infected siblings are the major reservoir of H. pylori in early and late childhood

demonstrating Protein Tyrosine Kinase inhibitor sustained intra-familial transmission of H. pylori. “
“Background: Helicobacter pylori colonize the mucus layer that covers the gastric epithelium and can cause gastritis, ulcers, and gastric cancer. Recently, Lactobacillus sp. have also been found to reside in this niche permanently. This study compares adhesive properties and proliferation of co-isolated lactobacilli and H. pylori in the presence of mucins and investigates

possibilities for lactobacilli-mediated inhibition of H. pylori. Materials and methods:  Binding and proliferation of four H. pylori and four Lactobacillus strains, simultaneously isolated after residing MCE in the stomachs of four patients for >4 years, to human gastric mucins were investigated using microtiter-based methods. Results:  The H. pylori strains co-isolated with lactobacilli exhibited the same mucin binding properties as demonstrated for H. pylori strains previously. In contrast, no binding to mucins was detected with the Lactobacillus strains. Proliferation of mucin-binding H. pylori strains was stimulated by the presence of mucins, whereas proliferation of non-binding H. pylori and Lactobacillus strains was unaffected. Associative cultures of co-isolated H. pylori and Lactobacillus strains showed no inhibition of H. pylori proliferation because of the presence of whole bacteria or supernatant of lactobacilli. Conclusions:  The presence of lactobacilli in the stomach did not select for different mucin binding properties of H. pylori, and Lactobacillus sp. did neither compete for binding sites nor inhibit the growth of co-isolated H. pylori. The effects of human gastric mucins on H. pylori proliferation vary between strains, and the host–bacteria interaction in the mucus niche thus depends on both the H. pylori strain and the microenvironment provided by the host mucins.