Race, African ancestry, and Helicobacter pylori infection in a low-income United States population.
BACKGROUND: Gastric cancer incidence in African Americans is twice that of whites, and differing prevalence of Helicobacter pylori strain-specific isolates may help explain the disparity. METHODS: Serum levels of antibodies to each of 15 H. pylori proteins were assessed using multiplex serology for a sample of 689 African American and white participants from the Southern Community Cohort Study. African and European admixture was estimated using a panel of 276 ancestry genetic markers, with "low," "medium," and "high" categories of African ancestry defined as <85%, 85% to 95%, and ≥95%. RESULTS: The majority (79%) of our study population were sero-positive for H. pylori. African American race was associated with a two- to sixfold increased odds for sero-positivity to eight H. pylori proteins, including the cancer-associated virulence constituents CagA [odds ratio (OR), 6.4; 95% CI, 4.5-9.1], and VacA (OR, 2.3; 95% CI, 1.5-3.5). Compared to whites, African Americans of low, medium, and high African ancestry had 1.6-, 4.1-, and 5.2-fold increased odds of sero-positivity to H. pylori, primarily related to CagA sero-positive strains, for which increasing African ancestry led to 2.5-, 9.6-, and 13.1-fold increased odds. Among African Americans alone, compared to those of low African ancestry, African Americans of medium and high African ancestry had 2.5- and 3.4-fold increased odds of sero-positivity to H. pylori, and 3.5- and 4.9-fold increased odds of CagA sero-positive H. pylori strains. CONCLUSIONS: Host genetic variation and/or lifestyle factors associated with African ancestry contribute to the likelihood of infection with H. pylori, particularly its virulent strains, in this low-income U.S. southern population. IMPACT: Our findings that low-income African Americans of high African ancestry have a particularly high prevalence of antibodies against H. pylori provides a framework for further research into better detection and prevention of gastric cancer in this population.
Epplein, M; Signorello, LB; Zheng, W; Peek, RM; Michel, A; Williams, SM; Pawlita, M; Correa, P; Cai, Q; Blot, WJ
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