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Sa1871 Phylogeographic Origin of Helicobacter pylori Determines Motility, Oxidative Stress and Virulence Responses Upon Coculture With Gastric Epithelial Cells
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degree relatives of GC patients (FDR), at high risk of GC and with different gastric precancerous lesions, in comparison with that in subjects of the general population (GP). Material and methods : Twenty-seven subjects with histological evidence of different levels of precancerous lesions, were submitted to gastroscopic examination with collection of gastric biopsies and HP culture: 14 were FDR and 13 were subjects from GP. Ten to 20 HP single colonies per biopsy, representing the possible HP genetic heterogeneity in the gastric niche, were analyzed for the presence of several cagPAI genes (CagA, CagE, VirB11) by PCR. Hom gene and VacA polymorphisms were also evaluated. Results : A total of 311 HP colonies were analysed. Concerning cagPAI genes, HP isolated from FDR showed lower genetic heterogeneity (three vs. six genotypes) and a more frequent intact cagPAI than GP (53.6 vs. 37.5, X22 = 69.9, p , .0001). The most frequent profile in HP from FDR was virB11 (+)/cagE(+)/cagA(+)/ vacAs1i1m1 (46.3% tested colonies) while s2i2m2 genotype was less represented (27.2% vs. 52.3%). HomB had a high frequency (78.2%) and was present in 71.4% of colonies with at least one CagIsland gene deletion. Conclusions : Strains isolated from FDR present a highly virulent genetic profile which can well represent the risk of these subjects to develop a severe disease.
AGA Abstracts
H. pylori Motility Promotes Preferential Colonization of Ulcerated Tissue in Mouse Stomach Eitaro Aihara, Andrea Matthis, Michael A. Schumacher, Yana Zavros, Karen ,. Ottemann, Marshall H. Montrose Background: The signals that drive H. pylori to successfully arrive at a colonization niche in gastric tissue are not understood, but are an essential first step for successful colonization, and ultimately the disease consequences of H. pylori infection. We asked if H. pylori can sense gastric ulceration tissue as a stimulus and tissue site to promote colonization, and if early colonization was dependent on the bacterial chemosensing that control flagellar motility. Aim: In the present study, we asked if H. pylori preferentially colonize ulcerated tissue rather than healthy tissue, and further tested colonization and effects on ulcer healing of isogenic bacterial mutants defective in flagellar rotation ( motB) or chemotaxis signal transduction (cheY). Methods: Topical application of acetic acid for 20-30 s to the stomach exterior induced an ulcer in anesthetized C57BL/6 mice. A single gavage of 106 -109 H. pylori was performed 2 days after ulcer induction. Ulcer size and number of bacteria colonizing normal and ulcerated stomach tissues were evaluated at 1 or 7 days after gavage. Results: 1 day after 108 inoculation, motile SS1 H. pylori colonized ulcerated corpus/fundus tissue (41.2 x 104 ± 11.9 x 104 CFU/g tissue) more than corresponding healthy tissue in the same stomachs (4.9 x 104 ± 1.9 x 104 CFU/g tissue, n=8, p,0.05). At 7 days, SS1 delayed ulcer healing (1.9 ± 0.6 mm2 ulcer) vs uninfected controls (0.3 ± 0.1 mm2 ulcer, p,0.05), but colonization was no longer different between healthy and ulcerated tissue. After a reduced inoculum (106), SS1 still preferentially colonized ulcerated tissue at 7 days as measured by CFU cultures (intact: 61.6 x 104 ± 28.2 x 104 CFU/g tissue vs ulcerated: 142.5 x 104 ± 46.2 x 104 CFU/g tissue, p,0.05) and real-time PCR of either 16S RNA/cDNA or the ssa gene as H. pylori markers. motB mutant SS1 H. pylori (106) did not colonize (healthy or ulcerated) tissue or delay ulcer healing. motB mutant SS1 H. pylori (108 -109) colonized in both areas (intact: 767.9 ± 896.6 CFU/g tissue vs ulcerated: 823.8 ± 903.4 CFU/g tissue, no significant different) without affecting ulcer healing. In contrast, H. pylori SS1 lacking cheY (106) was competent to colonize stomach tissue. At 7 days, the cheY mutant had delayed ulcer healing, but did not preferentially colonize ulcerated tissue (intact: 12.5 x 104 ± 12.6 x 104 CFU/g tissue vs ulcerated: 13.1 x 104 ± 6.2 x 104 CFU/g tissue, no significant different). Conclusion: H. pylori can rapidly and preferentially colonize sites of ulceration using chemotactic motility and subsequently slow ulcer repair. Lack of non-specific colonization by motB and cheY mutants suggests injury may release chemoattractants that determine the earliest H. pylori motility toward, and interactions with, host tissue.
Sa1871 Phylogeographic Origin of Helicobacter pylori Determines Motility, Oxidative Stress and Virulence Responses Upon Coculture With Gastric Epithelial Cells Alexander Sheh, Rupesh Chaturvedi, Douglas S. Merrell, Pelayo Correa, Keith T. Wilson, James G. Fox While Helicobacter pylori infects over 50% of the world's population, the mechanisms involved in the development of gastric disease are not fully understood. Bacterial, host and environmental factors play a role in disease outcome. To investigate the role of bacterial factors in H. pylori pathogenesis, global gene expression of six H. pylori isolates were analyzed during coculture with gastric epithelial cells. Clustering analysis of 6 Colombian clinical isolates from a region with low gastric cancer risk and a region with high gastric cancer risk, segregated strains based on their phylogeographic origin. 168 genes had increased expression in European strains while 360 genes had increased expression in African strains. Analysis of cell motility, virulence and oxidative stress response genes showed clear differences between African and European strains. European strains had greater expression of the virulence factors, cagA, vacA and babB and were associated with increased gastric histologic lesions in patients. African strains exhibited upregulation of motility genes. In AGS cells, European strains promoted significantly higher IL-8 expression compared to African strains. African strains significantly induced apoptosis whereas only one European strain significantly induced apoptosis. Our data suggest that gene expression profiles of clinical isolates can discriminate strains by phylogeographic origin and these profiles are associated with changes in expression of the proinflammatory and protumorigenic cytokine IL-8 and levels of apoptosis in host epithelial cells. These findings support the hypothesis that potential gene expression signatures may distinguish H. pylori strains from regions with higher gastric cancer incidence from regions with lesser risk.
Sa1869 Prevalence of Polymorphisms in Virulence Factor of Helicobacter pylori and Association With Gastroduodenal Diseases in South Korea Ji Yeon Kim, Nayoung Kim, Ryoung Hee Nam, Hyeon Jang, Yoon Jin Choi, Jung Won Lee, Dong Ho Lee, Hyun Chae Jung Background and aim: Helicobacter pylori (H. pylori) has been suggested to be associated with development of several gastroduodenal diseases. Clinical outcomes of H. pylori infection have been shown to be dependent on the variability of virulence factors in addition to host and environmental factors. The aims of this study were to evaluate the prevalence of each virulence factor and the association between polymorphisms in virulence factors of H. pylori and clinical outcome of gastroduodenal diseases in South Korea. In addition, the relationship of interleukin-8 (IL-8) and different virulence strains was evaluated. Methods: Three hundreds and seventy one H. pylori colonies were analyzed [66 colonies from 40 nonulcer dyspepsia (NUD) patients; 65 colonies from 36 benign gastric ulcer (BGU) patients; 101 colonies from 52 duodenal ulcer (DU) patients; 100 colonies from 62 stomach cancer (SC) patients; 39 colonies from 32 dysplasia patients]. PCR amplifications for vacA, cagA, iceA, oipA and dupA were performed using DNA extract from H. pylori isolates cultured from mucosal biopsy specimens. IL-8 was measured in high and low virulence strains by ELISA method. Results: Most colonies were composed with vacA s1 (97.8%), i1 (95.6%) and m1 (85.7%), cagA (84.7%), iceA1 (93.3%), oipA (88.9%) and dupA (93.4%) genotype. vacA s1 was frequent observed in DU (100.0%) and SC (100.0%) than NUD (93.9%) ( p=0.026). vacA i1 was also more frequent in DU (100.0%) than control (92.4%) ( p,0.001). iceA2 was less frequent in BGU (35.4%) than NUD (53.0%) ( p,0.001). oipA was highly detected in DU (95.0%) and SC (94.0%) than NUD (77.3%) ( p=0.001). dupA was higher in BGU (98.4%), DU (99.0%) and SC (98.4%) than NUD (72.5%) ( p,0.001). Infection by H. pylori with dupA had significant association with increasing risk of BGU (OR 45.24, 95% CI 3.21-638.24, p= 0.005), DU (OR 119.52, 95% CI 6.58-2170.30 p=0.001) and SC (OR 19.31, 95% CI 1.60232.53, p=0.020). vacA s1a2 showed increased risk of BGU (OR 10.52, 95% CI 1.71-64.58, p=0.011) and DU (OR 5.01, 95%CI 1.05-23.93, p=0.043). Whereas, iceA2 had protective effect on BGU (OR 0.05, 95% CI 0.01-0.32, p=0.001) and DU (OR 0.12, 95% CI 0.030.55, p=0.006). vacA i2 was also associated with decreasing risk of DU (OR 0.08, 95% CI 0.01-0.52, p=0.008). The mean level of IL-8 were 223.30±19.94 pg/mg in low virulence strains [dupA(-)&iceA2(+)] (n=6) and 247.49±34.28 pg/mg in high virulence strains [dupA(+)&iceA2(-)] (n=65) without significance. Conclusion: H. pylori in South Koreans was confirmed to be highly virulent [ vacA s1/i1/m1, cagA(+), iceA1(+), oipA(+) and dupA(+)]. dupA and vacA s1a2 were frequently associated with peptic ulcer disease, while iceA2 and vacA i2 seems to have protective effect on gastroduodenal diseases, especially in DU.
Sa1872 Helicobacter pylori cag+ Strains Induce Epithelial-Mesenchymal Transition via Activation of P120 Lydia E. Wroblewski, M. Blanca Piazuelo, Pelayo Correa, Albert B. Reynolds, Richard M. Peek Background: Helicobacter pylori infection is the strongest singular risk factor for gastric cancer. A microbial strain-specific constituent that induces epithelial responses with carcinogenic potential is the cag pathogenicity island, which encodes a secretion system that translocates bacterial effectors such as CagA into host cells. Increased cell migration, which we have previously shown to be induced by H. pylori in a cag-dependent manner, is a hallmark of transformed cells and represents one of the phenotypes that define the process of epithelial to mesenchymal transition (EMT). A host molecule implicated in regulation of EMT is the adherens junction protein p120-catenin (p120). During EMT, p120 undergoes an isoform transition or switch from short (isoform-3) to long (isoform-1), which is induced by Snail, and subsequently increases the risk of cancer. The aim of this study was to define mechanisms that regulate p120-dependent EMT within H. pylori-infected gastric epithelial cells. Methods: MKN28 human gastric epithelial cells or MKN28 cells stably transduced with p120-specific siRNA (MKN28 p120i) were co-cultured with the cag+ H. pylori strains 7.13 or 60190 or their corresponding isogenic cagE- mutants, which lack the ability to form a functional cag secretion system. Expression of the mesenchymal marker vimentin and the transcription factor Snail were determined by real-time RT-PCR and Western blot analysis. Expression of p120 isoforms was quantified via Western blot. Results: MKN28 cells infected with wildtype H. pylori expressed significantly (p,0.05) higher levels of vimentin and snail transcript compared to uninfected cells or cells infected with the corresponding H. pylori cagE- mutants. To define the role of p120 in EMT, MKN28 control or p120i cells were then infected with wild-type H. pylori. Loss of p120 significantly attenuated the ability of H. pylori to induce vimentin expression (5.9-fold vs. 2.9-fold induction, control vs. p120i, p ,0.05). Co-culture of MKN28 cells with wild-type H. pylori significantly increased expression levels (3.9-fold induction, p,0.05) of p120 isoform-1 compared to uninfected cells or cells infected with the isogenic cagE- mutants (0.7-fold induction). Induction of p120 isoform-1 by wild-type H. pylori was abolished in cells treated with Snail-specific siRNA. Conclusions: H. pylori induces EMT in a cag-dependent manner which is mediated via Snail, resulting in a novel p120 isoform switching pattern. These data identify cag-mediated signaling and p120 as key mediators of epithelial responses with carcinogenic potential that develop following infection by H. pylori.
Sa1870 Helicobacter pylori Virulence Factors in First Degree Relatives of Gastric Cancer Patients Renato Cannizzaro, Stefania Zanussi, Vincenzo Canzonieri, Giancarlo Basaglia, Valli De Re, Mara Fornasarig, Stefania Maiero, Enrico Orzes, Paolo De Paoli Background and aim : The presence of Helicobacter pylori (HP) virulence factors and family history play important roles in the pathogenesis of gastric cancer (GC) during a complex multi-step process. The aim of this study was to investigate the genomic HP profile in first
AGA Abstracts
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degree relatives of GC patients (FDR), at high risk of GC and with different gastric precancerous lesions, in comparison with that in subjects of the general population (GP). Material and methods : Twenty-seven subjects with histological evidence of different levels of precancerous lesions, were submitted to gastroscopic examination with collection of gastric biopsies and HP culture: 14 were FDR and 13 were subjects from GP. Ten to 20 HP single colonies per biopsy, representing the possible HP genetic heterogeneity in the gastric niche, were analyzed for the presence of several cagPAI genes (CagA, CagE, VirB11) by PCR. Hom gene and VacA polymorphisms were also evaluated. Results : A total of 311 HP colonies were analysed. Concerning cagPAI genes, HP isolated from FDR showed lower genetic heterogeneity (three vs. six genotypes) and a more frequent intact cagPAI than GP (53.6 vs. 37.5, X22 = 69.9, p , .0001). The most frequent profile in HP from FDR was virB11 (+)/cagE(+)/cagA(+)/ vacAs1i1m1 (46.3% tested colonies) while s2i2m2 genotype was less represented (27.2% vs. 52.3%). HomB had a high frequency (78.2%) and was present in 71.4% of colonies with at least one CagIsland gene deletion. Conclusions : Strains isolated from FDR present a highly virulent genetic profile which can well represent the risk of these subjects to develop a severe disease.
AGA Abstracts
H. pylori Motility Promotes Preferential Colonization of Ulcerated Tissue in Mouse Stomach Eitaro Aihara, Andrea Matthis, Michael A. Schumacher, Yana Zavros, Karen ,. Ottemann, Marshall H. Montrose Background: The signals that drive H. pylori to successfully arrive at a colonization niche in gastric tissue are not understood, but are an essential first step for successful colonization, and ultimately the disease consequences of H. pylori infection. We asked if H. pylori can sense gastric ulceration tissue as a stimulus and tissue site to promote colonization, and if early colonization was dependent on the bacterial chemosensing that control flagellar motility. Aim: In the present study, we asked if H. pylori preferentially colonize ulcerated tissue rather than healthy tissue, and further tested colonization and effects on ulcer healing of isogenic bacterial mutants defective in flagellar rotation ( motB) or chemotaxis signal transduction (cheY). Methods: Topical application of acetic acid for 20-30 s to the stomach exterior induced an ulcer in anesthetized C57BL/6 mice. A single gavage of 106 -109 H. pylori was performed 2 days after ulcer induction. Ulcer size and number of bacteria colonizing normal and ulcerated stomach tissues were evaluated at 1 or 7 days after gavage. Results: 1 day after 108 inoculation, motile SS1 H. pylori colonized ulcerated corpus/fundus tissue (41.2 x 104 ± 11.9 x 104 CFU/g tissue) more than corresponding healthy tissue in the same stomachs (4.9 x 104 ± 1.9 x 104 CFU/g tissue, n=8, p,0.05). At 7 days, SS1 delayed ulcer healing (1.9 ± 0.6 mm2 ulcer) vs uninfected controls (0.3 ± 0.1 mm2 ulcer, p,0.05), but colonization was no longer different between healthy and ulcerated tissue. After a reduced inoculum (106), SS1 still preferentially colonized ulcerated tissue at 7 days as measured by CFU cultures (intact: 61.6 x 104 ± 28.2 x 104 CFU/g tissue vs ulcerated: 142.5 x 104 ± 46.2 x 104 CFU/g tissue, p,0.05) and real-time PCR of either 16S RNA/cDNA or the ssa gene as H. pylori markers. motB mutant SS1 H. pylori (106) did not colonize (healthy or ulcerated) tissue or delay ulcer healing. motB mutant SS1 H. pylori (108 -109) colonized in both areas (intact: 767.9 ± 896.6 CFU/g tissue vs ulcerated: 823.8 ± 903.4 CFU/g tissue, no significant different) without affecting ulcer healing. In contrast, H. pylori SS1 lacking cheY (106) was competent to colonize stomach tissue. At 7 days, the cheY mutant had delayed ulcer healing, but did not preferentially colonize ulcerated tissue (intact: 12.5 x 104 ± 12.6 x 104 CFU/g tissue vs ulcerated: 13.1 x 104 ± 6.2 x 104 CFU/g tissue, no significant different). Conclusion: H. pylori can rapidly and preferentially colonize sites of ulceration using chemotactic motility and subsequently slow ulcer repair. Lack of non-specific colonization by motB and cheY mutants suggests injury may release chemoattractants that determine the earliest H. pylori motility toward, and interactions with, host tissue.
Sa1871 Phylogeographic Origin of Helicobacter pylori Determines Motility, Oxidative Stress and Virulence Responses Upon Coculture With Gastric Epithelial Cells Alexander Sheh, Rupesh Chaturvedi, Douglas S. Merrell, Pelayo Correa, Keith T. Wilson, James G. Fox While Helicobacter pylori infects over 50% of the world's population, the mechanisms involved in the development of gastric disease are not fully understood. Bacterial, host and environmental factors play a role in disease outcome. To investigate the role of bacterial factors in H. pylori pathogenesis, global gene expression of six H. pylori isolates were analyzed during coculture with gastric epithelial cells. Clustering analysis of 6 Colombian clinical isolates from a region with low gastric cancer risk and a region with high gastric cancer risk, segregated strains based on their phylogeographic origin. 168 genes had increased expression in European strains while 360 genes had increased expression in African strains. Analysis of cell motility, virulence and oxidative stress response genes showed clear differences between African and European strains. European strains had greater expression of the virulence factors, cagA, vacA and babB and were associated with increased gastric histologic lesions in patients. African strains exhibited upregulation of motility genes. In AGS cells, European strains promoted significantly higher IL-8 expression compared to African strains. African strains significantly induced apoptosis whereas only one European strain significantly induced apoptosis. Our data suggest that gene expression profiles of clinical isolates can discriminate strains by phylogeographic origin and these profiles are associated with changes in expression of the proinflammatory and protumorigenic cytokine IL-8 and levels of apoptosis in host epithelial cells. These findings support the hypothesis that potential gene expression signatures may distinguish H. pylori strains from regions with higher gastric cancer incidence from regions with lesser risk.
Sa1869 Prevalence of Polymorphisms in Virulence Factor of Helicobacter pylori and Association With Gastroduodenal Diseases in South Korea Ji Yeon Kim, Nayoung Kim, Ryoung Hee Nam, Hyeon Jang, Yoon Jin Choi, Jung Won Lee, Dong Ho Lee, Hyun Chae Jung Background and aim: Helicobacter pylori (H. pylori) has been suggested to be associated with development of several gastroduodenal diseases. Clinical outcomes of H. pylori infection have been shown to be dependent on the variability of virulence factors in addition to host and environmental factors. The aims of this study were to evaluate the prevalence of each virulence factor and the association between polymorphisms in virulence factors of H. pylori and clinical outcome of gastroduodenal diseases in South Korea. In addition, the relationship of interleukin-8 (IL-8) and different virulence strains was evaluated. Methods: Three hundreds and seventy one H. pylori colonies were analyzed [66 colonies from 40 nonulcer dyspepsia (NUD) patients; 65 colonies from 36 benign gastric ulcer (BGU) patients; 101 colonies from 52 duodenal ulcer (DU) patients; 100 colonies from 62 stomach cancer (SC) patients; 39 colonies from 32 dysplasia patients]. PCR amplifications for vacA, cagA, iceA, oipA and dupA were performed using DNA extract from H. pylori isolates cultured from mucosal biopsy specimens. IL-8 was measured in high and low virulence strains by ELISA method. Results: Most colonies were composed with vacA s1 (97.8%), i1 (95.6%) and m1 (85.7%), cagA (84.7%), iceA1 (93.3%), oipA (88.9%) and dupA (93.4%) genotype. vacA s1 was frequent observed in DU (100.0%) and SC (100.0%) than NUD (93.9%) ( p=0.026). vacA i1 was also more frequent in DU (100.0%) than control (92.4%) ( p,0.001). iceA2 was less frequent in BGU (35.4%) than NUD (53.0%) ( p,0.001). oipA was highly detected in DU (95.0%) and SC (94.0%) than NUD (77.3%) ( p=0.001). dupA was higher in BGU (98.4%), DU (99.0%) and SC (98.4%) than NUD (72.5%) ( p,0.001). Infection by H. pylori with dupA had significant association with increasing risk of BGU (OR 45.24, 95% CI 3.21-638.24, p= 0.005), DU (OR 119.52, 95% CI 6.58-2170.30 p=0.001) and SC (OR 19.31, 95% CI 1.60232.53, p=0.020). vacA s1a2 showed increased risk of BGU (OR 10.52, 95% CI 1.71-64.58, p=0.011) and DU (OR 5.01, 95%CI 1.05-23.93, p=0.043). Whereas, iceA2 had protective effect on BGU (OR 0.05, 95% CI 0.01-0.32, p=0.001) and DU (OR 0.12, 95% CI 0.030.55, p=0.006). vacA i2 was also associated with decreasing risk of DU (OR 0.08, 95% CI 0.01-0.52, p=0.008). The mean level of IL-8 were 223.30±19.94 pg/mg in low virulence strains [dupA(-)&iceA2(+)] (n=6) and 247.49±34.28 pg/mg in high virulence strains [dupA(+)&iceA2(-)] (n=65) without significance. Conclusion: H. pylori in South Koreans was confirmed to be highly virulent [ vacA s1/i1/m1, cagA(+), iceA1(+), oipA(+) and dupA(+)]. dupA and vacA s1a2 were frequently associated with peptic ulcer disease, while iceA2 and vacA i2 seems to have protective effect on gastroduodenal diseases, especially in DU.
Sa1872 Helicobacter pylori cag+ Strains Induce Epithelial-Mesenchymal Transition via Activation of P120 Lydia E. Wroblewski, M. Blanca Piazuelo, Pelayo Correa, Albert B. Reynolds, Richard M. Peek Background: Helicobacter pylori infection is the strongest singular risk factor for gastric cancer. A microbial strain-specific constituent that induces epithelial responses with carcinogenic potential is the cag pathogenicity island, which encodes a secretion system that translocates bacterial effectors such as CagA into host cells. Increased cell migration, which we have previously shown to be induced by H. pylori in a cag-dependent manner, is a hallmark of transformed cells and represents one of the phenotypes that define the process of epithelial to mesenchymal transition (EMT). A host molecule implicated in regulation of EMT is the adherens junction protein p120-catenin (p120). During EMT, p120 undergoes an isoform transition or switch from short (isoform-3) to long (isoform-1), which is induced by Snail, and subsequently increases the risk of cancer. The aim of this study was to define mechanisms that regulate p120-dependent EMT within H. pylori-infected gastric epithelial cells. Methods: MKN28 human gastric epithelial cells or MKN28 cells stably transduced with p120-specific siRNA (MKN28 p120i) were co-cultured with the cag+ H. pylori strains 7.13 or 60190 or their corresponding isogenic cagE- mutants, which lack the ability to form a functional cag secretion system. Expression of the mesenchymal marker vimentin and the transcription factor Snail were determined by real-time RT-PCR and Western blot analysis. Expression of p120 isoforms was quantified via Western blot. Results: MKN28 cells infected with wildtype H. pylori expressed significantly (p,0.05) higher levels of vimentin and snail transcript compared to uninfected cells or cells infected with the corresponding H. pylori cagE- mutants. To define the role of p120 in EMT, MKN28 control or p120i cells were then infected with wild-type H. pylori. Loss of p120 significantly attenuated the ability of H. pylori to induce vimentin expression (5.9-fold vs. 2.9-fold induction, control vs. p120i, p ,0.05). Co-culture of MKN28 cells with wild-type H. pylori significantly increased expression levels (3.9-fold induction, p,0.05) of p120 isoform-1 compared to uninfected cells or cells infected with the isogenic cagE- mutants (0.7-fold induction). Induction of p120 isoform-1 by wild-type H. pylori was abolished in cells treated with Snail-specific siRNA. Conclusions: H. pylori induces EMT in a cag-dependent manner which is mediated via Snail, resulting in a novel p120 isoform switching pattern. These data identify cag-mediated signaling and p120 as key mediators of epithelial responses with carcinogenic potential that develop following infection by H. pylori.
Sa1870 Helicobacter pylori Virulence Factors in First Degree Relatives of Gastric Cancer Patients Renato Cannizzaro, Stefania Zanussi, Vincenzo Canzonieri, Giancarlo Basaglia, Valli De Re, Mara Fornasarig, Stefania Maiero, Enrico Orzes, Paolo De Paoli Background and aim : The presence of Helicobacter pylori (HP) virulence factors and family history play important roles in the pathogenesis of gastric cancer (GC) during a complex multi-step process. The aim of this study was to investigate the genomic HP profile in first
AGA Abstracts
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