The seroprevalence of H. pylori in asymptomatic health check-up adult subjects in 2005 decreased to 59.6% from 66.9% in 1998, probably as a result of the improvement of socioeconomic status and hygiene.

BackgroundThe aim of this study was to evaluate the time trend of seropositivity of Helicobacter pylori (H. pylori) over the period of 13 years in an asymptomatic Korean population, and investigate associated risk factors.MethodsThis cross-sectional nationwide multicentre study surveyed anti-H. pylori IgG antibodies in 19,272 health check-up subjects (aged [greater than and equal to]16 years) in 2011. Risk factors for H. pylori infection were investigated using logistic regression. Seropositivity in asymptomatic subjects without H. pylori eradication was compared between the years 1998 and 2005. Birth cohort effects were also evaluated.ResultsAfter exclusion of subjects with a history of H. pylori eradication therapy (n = 3,712, 19.3%) and gastric symptoms (n = 4,764, 24.7%), the seroprevalence of H. pylori infection was 54.4% in 10,796 subjects. This was significantly lower than the seroprevalence of 59.6% in 2005 and that of 66.9% in 1998, and this decrease of seropositivity of H. pylori became widespread across all ages and in most areas of the country. This decreasing trend could be explained by cohort analysis. All younger birth cohorts had a lower seroprevalence of H. pylori than older birth cohorts at the same age. Decreased seroprevalence within the same birth cohorts also accounted for this phenomenon. Clinical risk factors of H. pylori infection were higher cholesterol level ([greater than and equal to] 240 mg/dl) (OR = 1.33; 95% CI = 1.14-1.54), male gender, older age, low income, and residence in a rural area.ConclusionsA decreasing trend of H. pylori seroprevalence due to a birth cohort effect requires further studies on its related human host factors as well as socio-economic and hygienic factors. In addition, the relationship between H. pylori infection and high cholesterol level needs more investigation regarding underlying pathogenesis.

TLR signaling is essential for intestinal tumorigenesis in Apcmin/+ mice, but the mechanisms by which this protein enhances tumor growth are unknown. Here we show that the Microflora-MyD88-ERK signaling in intestinal epithelial cells (IEC) promotes tumorigenesis by increasing the stability of the c-myc oncoprotein. Activation of ERK phosphorylates c-myc that prevents its ubiquitination and its subsequent proteasomal degradation. Accordingly, Apcmin/+/Myd88-/- mice display reduced levels of pERK and c-myc proteins in IEC, and a low incidence of IEC tumors. A MyD88-independent activation of ERK by EGF increases pERK and c-myc levels and restores the Min phenotype in Apcmin/+/Myd88-/- mice. Administration of an ERK inhibitor suppressed intestinal tumorigenesis in EGF-treated Apcmin/+/Myd88-/- and in Apcmin/+ mice and increased their survival. Our data reveal a new facet of oncogene-environment interaction, where the microflora-induced TLR activation regulates the expression of an oncogene that leads to IEC tumor growth in a susceptible host.

Endoscopic resection appears to be a safe and effective treatment for duodenal carcinoid tumors measuring ≤ 10 mm in diameter and confined to the submucosal layer.

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