(taken from the application) Helicobacter pylori (Hp) is a common worldwide infection; it is now known to be etiologically related to gastritis, peptic ulcer disease, gastric adenocarcinoma, and primary gastric lymphoma. The outcome of Hp infection differs among different ethnic groups. For example, in the United States although Hp infection is detected in all ethnic groups, gastric cancer is more common in Hispanics, Blacks, Vietnamese, Koreans, Japanese, and American Indians, compared to the white population. Possible factor(s) responsible for these differences include subtle distinctions in host or environmental factors (e.g., in diet) or differences in virulence in the common Hp strain(s) circulating within an ethnic group. While environmental or host factors are likely to be important, differences in virulence is a likely possibility because in many other bacterial diseases the expression of a disease can be directly related to specific virulence factors. Data from a number of laboratories suggest that different groups of Hp strains exist. Putative virulence markers, such as cagA and vacA genes and their protein products, have also been identified and they may be differentially present or expressed in different Hp-related gastrointestinal diseases. Our primary hypothesis is that different disease manifestations of Hp infection in different ethnic groups is a reflection of the heterogeneity and expression of different virulence factors in the predominant Hp strain(s) circulating in the ethnic group. The specific objectives of this study are: To determine whether the presence of Hp virulence factors, including genetic and/or phenotypic variations in Hp isolates within different ethnic groups in the US, can be correlated with severity, extent, or pattern of gastritis. We also plan to use the DNA fingerprinting method, REP-PCR, to assess genetic similarity among Hp isolates within and between different ethnic groups. This study will also determine whether differences in prevalence and heterogeneity of specific candidate virulence factors may be the underlying mechanism leading to differences in the extent and severity of Hp-related gastric damage and diseases in different ethnic groups in the United States.
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