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1
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0036370334
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Helicobacter pylori and gastrointestinal tract adenocarcinomas
-
Peek RM Jr, Blaser MJ. Helicobacter pylori and gastrointestinal tract adenocarcinomas. Nat Rev Cancer 2002; 2:28-37.
-
(2002)
Nat Rev Cancer
, vol.2
, pp. 28-37
-
-
Peek Jr., R.M.1
Blaser, M.J.2
-
3
-
-
17644415392
-
The sialic acid binding SabA adhesin of Helicobacter pylori is essential for nonopsonic activation of human neutrophils
-
Unemo M, Aspholm-Hurtig M, Ilver D, et al. The sialic acid binding SabA adhesin of Helicobacter pylori is essential for nonopsonic activation of human neutrophils. J Biol Chem 2005; 280:15390-15397.
-
(2005)
J Biol Chem
, vol.280
, pp. 15390-15397
-
-
Unemo, M.1
Aspholm-Hurtig, M.2
Ilver, D.3
-
4
-
-
2442502597
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Helicobacter pylori interacts with the human single-domain trefoil protein TFF1
-
USA
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Clyne M, Dillon P, Daly S, et al. Helicobacter pylori interacts with the human single-domain trefoil protein TFF1. Proc Natl Acad Sci USA 2004; 101:7409-7414. This paper describes important studies indicating that TFF1 binds H. pylori and, therefore, may serve as a receptor for H. pylori and explain the tropism of H. pylori within gastric tissue.
-
(2004)
Proc Natl Acad Sci
, vol.101
, pp. 7409-7414
-
-
Clyne, M.1
Dillon, P.2
Daly, S.3
-
5
-
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4043099127
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Natural antibiotic function of a human gastric mucin against Helicobacter pylori infection
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Kawakubo M, Ito Y, Okimura Y, et al. Natural antibiotic function of a human gastric mucin against Helicobacter pylori infection. Science 2004; 305:1003-1006. This paper reports that specific O-glycans are produced by gastric mucous cells deep in the glandular regions where H. pylori is rarely found. These O-glycans exert an antimicrobial effect on H. pylori by inhibiting biosynthesis of a major cell-wall component.
-
(2004)
Science
, vol.305
, pp. 1003-1006
-
-
Kawakubo, M.1
Ito, Y.2
Okimura, Y.3
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6
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4544330058
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Gastric transcription profile of Helicobacter pylori infection in the rhesus macaque
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Huff JL, Hansen LM, Solnick JV. Gastric transcription profile of Helicobacter pylori infection in the rhesus macaque. Infect Immun 2004; 72:5216-5226.
-
(2004)
Infect Immun
, vol.72
, pp. 5216-5226
-
-
Huff, J.L.1
Hansen, L.M.2
Solnick, J.V.3
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7
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7644230745
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Profiling of microdissected gastric epithelial cells reveals a cell type-specific response to Helicobacter pylori infection
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Mueller A, Merrell DS, Grimm J, Falkow S. Profiling of microdissected gastric epithelial cells reveals a cell type-specific response to Helicobacter pylori infection. Gastroenterology 2004; 127:1446-1462. Gene-expression profiles of three gastric epithelial cell lineages were examined in response to H. pylori colonization. Only gastric mucous cells mounted a specific response to H. pylori.
-
(2004)
Gastroenterology
, vol.127
, pp. 1446-1462
-
-
Mueller, A.1
Merrell, D.S.2
Grimm, J.3
Falkow, S.4
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8
-
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0035923621
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Helicobacter pylori arginase inhibits nitric oxide production by eukaryotic cells: A strategy for bacterial survival
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USA
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Gobert AP, McGee DJ, Akhtar M, et al. Helicobacter pylori arginase inhibits nitric oxide production by eukaryotic cells: a strategy for bacterial survival. Proc Natl Acad Sci USA 2001; 98:13844-13849.
-
(2001)
Proc Natl Acad Sci
, vol.98
, pp. 13844-13849
-
-
Gobert, A.P.1
McGee, D.J.2
Akhtar, M.3
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9
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19944430187
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Spermine causes loss of innate immune response to Helicobacter pylori by inhibition of inducible nitric-oxide synthase translation
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Bussiere FI, Chaturvedi R, Cheng Y, et al. Spermine causes loss of innate immune response to Helicobacter pylori by inhibition of inducible nitric-oxide synthase translation. J Biol Chem 2005; 280:2409-2412. This paper reports that H. pylori induces both arginase II and ornithine decarboxylase, leading to the production of spermine which inhibits inducible NO synthase, limiting the production of bactericidal nitric oxide.
-
(2005)
J Biol Chem
, vol.280
, pp. 2409-2412
-
-
Bussiere, F.I.1
Chaturvedi, R.2
Cheng, Y.3
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10
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20444491996
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Helicobacter pylori-induced macrophage apoptosis requires activation of ornithine decarboxylase by c-Myc
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Cheng Y, Chaturvedi R, Asim M, et al. Helicobacter pylori-induced macrophage apoptosis requires activation of ornithine decarboxylase by c-Myc. J Biol Chem 2005; 280:22492-22496.
-
(2005)
J Biol Chem
, vol.280
, pp. 22492-22496
-
-
Cheng, Y.1
Chaturvedi, R.2
Asim, M.3
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11
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4444300887
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2 increase AP endonuclease-1/redox factor-1 expression in human gastric epithelial cells
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2 increase AP endonuclease-1/redox factor-1 expression in human gastric epithelial cells. Gastroenterology 2004; 127:845-858. This important article reports induction of APE-1/Ref-1, an enzyme that repairs damaged DNA and can activate transcription factors, in response to H. pylori, both in vitro and in vivo, suggesting a role for APE-1/Ref-1 in H. pylori pathogenesis.
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(2004)
Gastroenterology
, vol.127
, pp. 845-858
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Ding, S.Z.1
O'Hara, A.M.2
Denning, T.L.3
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12
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2942729762
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Helicobacter pylori arginase inhibits T cell proliferation and reduces the expression of the TCR ζ-chain (CD3ζ)
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Zabaleta J, McGee DJ, Zea AH, et al. Helicobacter pylori arginase inhibits T cell proliferation and reduces the expression of the TCR ζ-chain (CD3ζ). J Immunol 2004; 173:586-593. These studies suggest that, in addition to metabolizing arginine to urea, the H. pylori arginase RocF may also impair T-cell function.
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(2004)
J Immunol
, vol.173
, pp. 586-593
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Zabaleta, J.1
McGee, D.J.2
Zea, A.H.3
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13
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1842477039
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Helicobacter pylori-specific antibodies impair the development of gastritis, facilitate bacterial colonization, and counteract resistance against infection
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Akhiani AA, Schon K, Franzen LE, et al. Helicobacter pylori-specific antibodies impair the development of gastritis, facilitate bacterial colonization, and counteract resistance against infection. J Immunol 2004; 172:5024-5033.
-
(2004)
J Immunol
, vol.172
, pp. 5024-5033
-
-
Akhiani, A.A.1
Schon, K.2
Franzen, L.E.3
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14
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20444377718
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IgA antibodies impair resistance against Helicobacter pylori infection: Studies on immune evasion in IL-10-deficient mice
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Akhiani AA, Stensson A, Schon K, Lycke NY. IgA antibodies impair resistance against Helicobacter pylori infection: studies on immune evasion in IL-10-deficient mice. J Immunol 2005; 174:8144-8153. Using interleukin-10-, IgA-, and interleukin-10/IgA-deficient mice, these experiments demonstrated that absence of interleukin-10 and IgA both led to decreased H. pylori colonization densities and increased levels of inflammation, indicating a role for the molecules in H. pylori persistence.
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(2005)
J Immunol
, vol.174
, pp. 8144-8153
-
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Akhiani, A.A.1
Stensson, A.2
Schon, K.3
Lycke, N.Y.4
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15
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0344234277
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Helicobacter pylori flagellins have very low intrinsic activity to stimulate human gastric epithelial cells via TLR5
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Lee SK, Stack A, Katzowitsch E, et al. Helicobacter pylori flagellins have very low intrinsic activity to stimulate human gastric epithelial cells via TLR5. Microbes Infect 2003; 5:1345-1356.
-
(2003)
Microbes Infect
, vol.5
, pp. 1345-1356
-
-
Lee, S.K.1
Stack, A.2
Katzowitsch, E.3
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16
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2442678870
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Helicobacter pylori flagellin evades Toll-like receptor 5-mediated innate immunity
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Gewirtz AT, Yu Y, Krishna US, et al. Helicobacter pylori flagellin evades Toll-like receptor 5-mediated innate immunity. J Infect Dis 2004; 189:1914-1920.
-
(2004)
J Infect Dis
, vol.189
, pp. 1914-1920
-
-
Gewirtz, A.T.1
Yu, Y.2
Krishna, U.S.3
-
17
-
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21544448078
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Evasion of Toll-like receptor 5 by flagellated bacteria
-
USA
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Andersen-Nissen E, Smith KD, Strobe KL, et al. Evasion of Toll-like receptor 5 by flagellated bacteria. Proc Natl Acad Sci USA 2005; 102:9247-9252.
-
(2005)
Proc Natl Acad Sci
, vol.102
, pp. 9247-9252
-
-
Andersen-Nissen, E.1
Smith, K.D.2
Strobe, K.L.3
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18
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2542510727
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Expression and subcellular distribution of toll-like receptors TLR4, TLR5 and TLR9 on the gastric epithelium in Helicobacter pylori infection
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Schmausser B, Andrulis M, Endrich S, et al. Expression and subcellular distribution of toll-like receptors TLR4, TLR5 and TLR9 on the gastric epithelium in Helicobacter pylori infection. Clin Exp Immunol 2004; 136:521-526. This paper reports the subcellular redistribution of TLR5 and TLR9 within the context of H. pylori infection.
-
(2004)
Clin Exp Immunol
, vol.136
, pp. 521-526
-
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Schmausser, B.1
Andrulis, M.2
Endrich, S.3
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19
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5044240576
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Intact gram-negative Helicobacter pylori, Helicobacter felis, and Helicobacter hepaticus bacteria activate innate immunity via toll-like receptor 2 but not toll-like receptor 4
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Mandell L, Moran AP, Cocchiarella A, et al. Intact gram-negative Helicobacter pylori, Helicobacter felis, and Helicobacter hepaticus bacteria activate innate immunity via toll-like receptor 2 but not toll-like receptor 4. Infect Immun 2004; 72:6446-6454.
-
(2004)
Infect Immun
, vol.72
, pp. 6446-6454
-
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Mandell, L.1
Moran, A.P.2
Cocchiarella, A.3
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20
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21544441173
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NF-κB activation and potentiation of proinflammatory responses by the Helicobacter pylori CagA protein
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USA
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Brandt S, Kwok T, Hartig R, et al. NF-κB activation and potentiation of proinflammatory responses by the Helicobacter pylori CagA protein. Proc Natl Acad Sci USA 2005; 102:9300-9305.
-
(2005)
Proc Natl Acad Sci
, vol.102
, pp. 9300-9305
-
-
Brandt, S.1
Kwok, T.2
Hartig, R.3
-
21
-
-
23044463653
-
Activation of β-catenin by carcinogenic Helicobacter pylori
-
USA
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Franco AT, Israel DA, Washington MK, et al. Activation of β-catenin by carcinogenic Helicobacter pylori. Proc Natl Acad Sci USA 2005; 102:10646-10651.
-
(2005)
Proc Natl Acad Sci
, vol.102
, pp. 10646-10651
-
-
Franco, A.T.1
Israel, D.A.2
Washington, M.K.3
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22
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22144474386
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Functional antagonism between Helicobacter pylori CagA and vacuolating toxin VacA in control of the NFAT signaling pathway in gastric epithelial cells
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USA
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Yokoyama K, Higashi H, Ishikawa S, et al. Functional antagonism between Helicobacter pylori CagA and vacuolating toxin VacA in control of the NFAT signaling pathway in gastric epithelial cells. Proc Natl Acad Sci USA 2005; 102:9661-9666. This study describes the roles of CagA and VacA in regulating the NFAT signaling pathway in response to H. pylori. Results indicate that phosphorylated CagA activated NFAT whereas treatment with VacA inhibited this activation.
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(2005)
Proc Natl Acad Sci
, vol.102
, pp. 9661-9666
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Yokoyama, K.1
Higashi, H.2
Ishikawa, S.3
-
23
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9244245293
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Nod1 responds to peptidoglycan delivered by the Helicobacter pylori cag pathogenicity island
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Viala J, Chaput C, Boneca IG, et al. Nod1 responds to peptidoglycan delivered by the Helicobacter pylori cag pathogenicity island. Nat Immunol 2004; 5:1166-1174. These studies demonstrated that H. pylori peptigoglycan is delivered by the type IV cag secretion system, which is then recognized by the intracellular receptor Nod1, leading to NF-κB activation. Further in-vivo studies showed an important role for Nod1 in host defense against H. pylori.
-
(2004)
Nat Immunol
, vol.5
, pp. 1166-1174
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Viala, J.1
Chaput, C.2
Boneca, I.G.3
-
24
-
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0042932364
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Helicobacter pylori vacuolating cytotoxin inhibits T lymphocyte activation
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Gebert B, Fischer W, Weiss E, et al. Helicobacter pylori vacuolating cytotoxin inhibits T lymphocyte activation. Science 2003; 301:1099-1102.
-
(2003)
Science
, vol.301
, pp. 1099-1102
-
-
Gebert, B.1
Fischer, W.2
Weiss, E.3
-
25
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2442682964
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Inhibition of primary human T cell proliferation by Helicobacter pylori vacuolating toxin (VacA) is independent of VacA effects on IL-2 secretion
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USA
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Sundrud MS, Torres VJ, Unutmaz D, Cover TL. Inhibition of primary human T cell proliferation by Helicobacter pylori vacuolating toxin (VacA) is independent of VacA effects on IL-2 secretion. Proc Natl Acad Sci USA 2004; 101:7727-7732. This report demonstrates that VacA inhibits the expansion of activated T cells, allowing evasion of the adaptive immune response.
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(2004)
Proc Natl Acad Sci
, vol.101
, pp. 7727-7732
-
-
Sundrud, M.S.1
Torres, V.J.2
Unutmaz, D.3
Cover, T.L.4
-
26
-
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5044224294
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Molecular biology of gastric cancer: Helicobacter infection and gastric adenocarcinoma: bacterial and host factors responsible for altered growth signaling
-
Stoicov C, Saffari R, Cai X, et al. Molecular biology of gastric cancer: Helicobacter infection and gastric adenocarcinoma: bacterial and host factors responsible for altered growth signaling. Gene 2004; 341:1-17.
-
(2004)
Gene
, vol.341
, pp. 1-17
-
-
Stoicov, C.1
Saffari, R.2
Cai, X.3
-
27
-
-
20444414899
-
Intestinal helminthiasis in Colombian children promotes a Th2 response to Helicobacter pylori: Possible implications for gastric carcinogenesis
-
Whary MT, Sundina N, Bravo LE, et al. Intestinal helminthiasis in Colombian children promotes a Th2 response to Helicobacter pylori: possible implications for gastric carcinogenesis. Cancer Epidemiol Biomarkers Prev 2005; 14:1464-1469.
-
(2005)
Cancer Epidemiol Biomarkers Prev
, vol.14
, pp. 1464-1469
-
-
Whary, M.T.1
Sundina, N.2
Bravo, L.E.3
-
28
-
-
23344447799
-
Slow genetic divergence of Helicobacter pylori strains during long-term colonization
-
Lundin A, Bjorkholm B, Kupershmidt I, et al. Slow genetic divergence of Helicobacter pylori strains during long-term colonization. Infect Immun 2005; 73:4818-4822.
-
(2005)
Infect Immun
, vol.73
, pp. 4818-4822
-
-
Lundin, A.1
Bjorkholm, B.2
Kupershmidt, I.3
-
29
-
-
13444261202
-
Host adaptation and immune modulation are mediated by homologous recombination in Helicobacter pylori
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Robinson K, Loughlin MF, Potter R, Jenks PJ. Host adaptation and immune modulation are mediated by homologous recombination in Helicobacter pylori. J Infect Dis 2005; 191:579-587. Using a wild-type and an isogenic mutant H. pylori strain deficient in homologous recombination this study demonstrated the importance of recombination in the provocation of a Th2 response and persistence in an in-vivo model of infection.
-
(2005)
J Infect Dis
, vol.191
, pp. 579-587
-
-
Robinson, K.1
Loughlin, M.F.2
Potter, R.3
Jenks, P.J.4
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