AIM: To investigate the influence of the CagA diversity in Helicobacter pylori (H. pylori ) strains from Colombia on the host cell biology. METHODS: Eighty-four H. pylori-cagA positive strains with different Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs patterns, isolated from patients with gastritis (n=17), atrophic gastritis (n=17), duodenal ulcer (n=16), intestinal metaplasia (n=16) and gastric cancer (n=18), were included. To determine the integrity of the cag pathogenicity island (cag PAI) we evaluated the presence of cagA, cagT, cagE, and cag10 genes by polymerase chain reaction. AGS gastric epithelial cellswere infected with each strain and assayed for translo-cation and tyrosine phosphorylation of CagA by western blot, secretion of interleukin-8 (IL-8) by enzyme-linked immuno sorbent assay after taking supernatants from cocultures and cell elongation induction. For cell elongation quantification, coculture photographs were taken and the proportion of “hummingbird” cells (>15 μm) was determined. RESULTS: Overall 72% (60/84) of the strains were found to harbor a functional cag PAI. Levels of phos-phorylated CagA were significantly higher for isolates from duodenal ulcer than the ones in strains from gas-tritis, atrophic gastritis, intestinal metaplasia and gastric cancer (49.1% ± 23.1% vs 21.1% ± 19.5%, P < 0.02; 49.1% ± 23.1% vs 26.2%±14.8%, P<0.045; 49.1% ± 23.1% vs 21.5% ± 19.5%, P<0.043 and 49.1% ± 23.1% vs 29.5% ± 27.1%, P < 0.047 respectively). We observed variable IL-8 expression levels ranging from 0 to 810 pg/mL and from 8.8 to 1442 pg/mL at 6 h and 30 h post-infection, respectively. cagPAI-defective strains did not induce detectable levels of IL-8 at 6 h post-infection. At 30 h post-infection all strains induced IL-8 expression in AGS cells, although cagPAI-defective strains induced significantly lower levels of IL-8 than strains with a functional cagPAI (57.1 ± 56.6 pg/mL vs 513.6 ± 338.6 pg/mL,P < 0.0001). We did not observe differences in the extent of cell elongation induction between strains with a functional or a defective cagPAI in 6 h cocultures. At 24 h post infection strains with functionalcagPAI showed high diversity in the extent of hummingbird phenotype induction ranging from 7% to 34%. cag PAI defective strains induced significantly lower levels of elongation than strains with functional cag-PAI with one or more than one EPIYA-C motif (15.1% ± 5.2%vs 18.9% ± 4.7%,P < 0.03; and 15.1% ± 5.2% vs 20.0% ± 5.1%, P < 0.003 respectively). No differences were observed in cellular elongation inductionor IL-8 expression among H. pylori strains bearing one and more than one EPIYA-C motifs, neither at 6 h nor at 24 h of coculture. There were no associations between the levels of induction of cell elongation or IL-8 expression and number of EPIYA motifs or pathology. CONCLUSION: The present work describes a lack of association between H. pylori CagA protein EPIYA motifs variations from Colombian isolates and disease-associated cellular responses. AIM: To investigate the influence of the CagA diversity in Helicobacter pylori (H. pylori) strain from Colombia on the host cell biology. METHODS: Eighty-four H. pylori-cagA positive strain with different Glu-Pro-Ile- Tyr-Ala (EPIYA) motifs patterns from isolated patients with gastritis (n = 17), atrophic gastritis (n = 17), duodenal ulcer (n = 16), intestinal metaplasia included. To determine the integrity of the cag pathogenicity island (cag PAI) we evaluated the presence of cagA, cagT, cagE, and cag10 genes by polymerase chain reaction. AGS gastric epithelial cells were infected with each strain and assayed for translo-cation and tyrosine phosphorylation of CagA by western blot, secretion of interleukin-8 (IL-8) by enzyme-linked immuno sorbent assay after taking supernatants from cocultures and cell elongation induction. For cell elongation quantification, coculture photographs were taken and the proportion of “hummingbird ”cells (> 15 μm) was de RESULTS: Overall 72% (60/84) of the strains were found to harbor a functional cag PAI. Levels of phos-phorylated CagA were significantly higher for isolates from duodenal ulcer than the ones in in from gas-tritis, atrophic gastritis , 49.1% ± 23.1% vs 21.5% ± 19.5%, P <0.02; 49.1% ± 23.1% vs 26.2% ± 14.8%, P <0.045; , P <0.043 and 49.1% ± 23.1% vs 29.5% ± 27.1%, P <0.047 respectively). We observed that IL-8 expression levels ranging from 0 to 810 pg / mL and from 8.8 to 1442 pg / mL at 6 h At 30 h post-infection, respectively. cagPAI-defective expression did not induce detectable levels of IL-8 at 6 h post-infection. At 30 h post-infection all induced IL-8 expression in AGS cells, although cagPAI-defective We did not observe differences in the ex-expression of IL-8 than with a functional cagPAI (57.1 ± 56.6 pg / mL vs 513.6 ± 338.6 pg / mL, P <0.0001) tent of cell elongation induction between strains with a functional or a defective cagPAI in 6 h cocultures. At 24 h post infection strain with functionalcagPAI showed high diversity in the extent of hummingbird phenotype induction ranging from 7% to 34%. levels of elongation than with functional cag-PAI with one or more than one EPIYA-C motif (15.1% ± 5.2% vs 18.9% ± 4.7%, P <0.03; and 15.1% ± 5.2% vs 20.0% ± 5.1% P <0.003 respectively). No differences were observed in the cellular elongation induction of IL-8 expression among H. pylori strains bearing one and more than one EPIYA-C motifs, neither at 6 h nor at 24 h of coculture. There were no associations between the levels of induction of cell elongation or IL-8 expression and number of EPIYA motifs or pathology. CONCLUSION: The present work describes a lack of association between H. pylori CagA protein EPIYA motifs variations from Colombian isolates and disease-associated cellular responses.