摘要
AIM:To evaluate the influence of MUC1 mucin variable number of tandem repeats (VNTR) variability on H pylori adhesion to gastric cells. METHODS: Enzyme linked immunosorbent assay (ELISA)-based adhesion assays were performed to measure the adhesion of different H pylori strains (HP26695 and HPTx30a) to gastric carcinoma cell lines (GP202 and MKN45) and GP202 clones expressing recombinant MUC1 with different VNTR lengths. RESULTS: Evaluation of adhesion results shows that H pylori pathogenic strain HP26695 has a significantly higher (P < 0.05) adhesion to all the cell lines and clones tested, when compared to the non-pathogenic strain HPTx30a. Bacteria showed a significantly higher (P < 0.05) adhesion to the GP202 cell line, when compared to the MKN45 cell line. Furthermore, both strains showed a significantly higher (P < 0.05) adhesion to GP202 clones with larger MUC1 VNTR domains. CONCLUSION: This work shows that MUC1 mucin variability conditions H pylori binding to gastric cells. The extent of bacterial adhesion depends on the size of theMUC1 VNTR domain. The adhesion is further dependent on bacterial pathogenicity and the gastric cell line. MUC1 mucin variability may contribute to determine H pylori colonization of the gastric mucosa.
AIM：To evaluate the influence of MUC1 mucin variable number of tandem repeats （VNTR） variability on H pylori adhesion to gastric cells. METHODS： Enzyme linked immunosorbent assay （ELISA）-based adhesion assays were performed to measure the adhesion of different H pylori strains （HP26695 and HPTx30a） to gastric carcinoma cell lines （GP202 and MKN45） and GP202 clones expressing recombinant MUC1 with different VNTR lengths. RESULTS： Evaluation of adhesion results shows that H pylori pathogenic strain HP26695 has a significantly higher （P 〈 0.05） adhesion to all the cell lines and clones tested, when compared to the non-pathogenic strain HPTx30a. Bacteria showed a significantly higher （P 〈 0.05） adhesion to the GP202 cell line, when compared to the MKN45 cell line. Furthermore, both strains showed a significantly higher （P 〈 0.05） adhesion to GP202 clones with larger MUC1 VNTR domains. CONCLUSION： This work shows that MUC1 mucin variability conditions H pylori binding to gastric cells. The extent of bacterial adhesion depends on the size of theMUC1 VNTR domain. The adhesion is further dependent on bacterial pathogenicity and the gastric cell line. MUC1 mucin variability may contribute to determine H pylori colonization of the gastric mucosa.
基金
Portuguese Foundation for Science and Technology(FCT)
Project POCTI/CBO/44812/2002
Project POCTI/SAU-IMI/56895/2004
National Institutes of Health, R01-CA57362
