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We determined whether chronic\n                    <jats:italic>H. pylori<\/jats:italic>\n                    infection induced mutations in the gastric mucosa of male and female\n                    <jats:italic>gpt<\/jats:italic>\n                    delta C57BL\/6 mice infected for 6 or 12 mo. Point mutations were increased in females infected for 12 mo. The mutation frequency in this group was 1.6-fold higher than in uninfected mice of both sexes (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.05). A:T-to-G:C transitions and G:C-to-T:A transversions were 3.8 and 2.0 times, respectively, more frequent in this group than in controls. Both mutations are consistent with DNA damage induced by oxidative stress. No increase in the frequency of deletions was observed. Females had more severe gastric lesions than males at 6 mo postinfection (MPI;\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.05), but this difference was absent at 12 MPI. In all mice, infection significantly increased expression of\n                    <jats:italic>IFN<\/jats:italic>\n                    \u03b3,\n                    <jats:italic>IL-17<\/jats:italic>\n                    ,\n                    <jats:italic>TNF<\/jats:italic>\n                    \u03b1, and\n                    <jats:italic>iNOS<\/jats:italic>\n                    at 6 and 12 mo, as well as\n                    <jats:italic>H. pylori<\/jats:italic>\n                    \u2013specific IgG1 levels at 12 MPI (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.05) and IgG2c levels at 6 and 12 MPI (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.01 and\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.001). At 12 MPI, IgG2c levels in infected females were higher than at 6 MPI (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.05) and also than those in infected males at 12 MPI (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.05). Intensity of responses was mediated by sex and duration of infection. Lower\n                    <jats:italic>H. pylori<\/jats:italic>\n                    colonization indicated a more robust host response in females than in males. Earlier onset of severe gastric lesions and proinflammatory, Th1-biased responses in female C57BL\/6 mice may have promoted mutagenesis by exposing the stomach to prolonged oxidative stress.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1009017107","type":"journal-article","created":{"date-parts":[[2010,8,10]],"date-time":"2010-08-10T23:23:55Z","timestamp":1281482635000},"page":"15217-15222","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":39,"title":["Mutagenic potency of\n                    <i>Helicobacter pylori<\/i>\n                    in the gastric mucosa of mice is determined by sex and duration of infection"],"prefix":"10.1073","volume":"107","author":[{"given":"Alexander","family":"Sheh","sequence":"first","affiliation":[{"name":"Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chung Wei","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139;"},{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02139; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenichi","family":"Masumura","sequence":"additional","affiliation":[{"name":"Division of Genetics and Mutagenesis, National Institute of Health Sciences, Tokyo 158-8501, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barry H.","family":"Rickman","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02139; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takehiko","family":"Nohmi","sequence":"additional","affiliation":[{"name":"Division of Genetics and Mutagenesis, National Institute of Health Sciences, Tokyo 158-8501, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerald N.","family":"Wogan","sequence":"additional","affiliation":[{"name":"Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James G.","family":"Fox","sequence":"additional","affiliation":[{"name":"Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139;"},{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02139; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David B.","family":"Schauer","sequence":"additional","affiliation":[{"name":"Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139;"},{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02139; and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2010,8,10]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI30111"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra020542"},{"key":"e_1_3_3_3_2","first-page":"1","article-title":"Schistosomes, liver flukes and Helicobacter pylori. 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