{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T01:03:05Z","timestamp":1788915785843,"version":"build-2803163510"},"reference-count":40,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2010,1,1]],"date-time":"2010-01-01T00:00:00Z","timestamp":1262304000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2010,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    is recognized as an etiological agent of gastroduodenal diseases.\n                    <jats:italic>H. pylori<\/jats:italic>\n                    produces various toxic substances, including lipopolysaccharide (LPS). However,\n                    <jats:italic>H. pylori<\/jats:italic>\n                    LPS exhibits extremely weakly endotoxic activity compared to the typical LPS, such as that produced by\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    , which acts through Toll-like receptor 4 (TLR4) to induce inflammatory molecules. The gastric epithelial cell lines MKN28 and MKN45 express TLR4 at very low levels, so they show very weak interleukin-8 (IL-8) production in response to\n                    <jats:italic>E. coli<\/jats:italic>\n                    LPS, but pretreatment with\n                    <jats:italic>H. pylori<\/jats:italic>\n                    LPS markedly enhanced IL-8 production induced by\n                    <jats:italic>E. coli<\/jats:italic>\n                    LPS by upregulating TLR4 via TLR2 and the MEK1\/2-ERK1\/2 pathway. The transcription factor NF-Y was activated by this signal and promoted transcription of the\n                    <jats:italic>tlr4<\/jats:italic>\n                    gene. These MEK1\/2-ERK1\/2 signal-mediated activities were more potently activated by LPS carrying a weakly antigenic epitope, which is frequently found in gastric cancers, than by LPS carrying a highly antigenic epitope, which is associated with chronic gastritis.\n                    <jats:italic>H. pylori<\/jats:italic>\n                    LPS also augmented the proliferation rate of gastric epithelial cells via the MEK1\/2-ERK1\/2 pathway.\n                    <jats:italic>H. pylori<\/jats:italic>\n                    LPS may be a pathogenic factor causing gastric tumors by enhancing cell proliferation and inflammation via the MEK1\/2-ERK1\/2 mitogen-activated protein kinase cascade in gastric epithelial cells.\n                  <\/jats:p>","DOI":"10.1128\/iai.00903-09","type":"journal-article","created":{"date-parts":[[2009,10,26]],"date-time":"2009-10-26T21:29:57Z","timestamp":1256592597000},"page":"468-476","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":94,"title":["<i>Helicobacter pylori<\/i>\n                    Lipopolysaccharides Upregulate Toll-Like Receptor 4 Expression and Proliferation of Gastric Epithelial Cells via the MEK1\/2-ERK1\/2 Mitogen-Activated Protein Kinase Pathway"],"prefix":"10.1128","volume":"78","author":[{"given":"Shin-ichi","family":"Yokota","sequence":"first","affiliation":[{"name":"Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku, Sapporo 060-8556, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tamaki","family":"Okabayashi","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku, Sapporo 060-8556, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Rehli","sequence":"additional","affiliation":[{"name":"Department of Hematology and Oncology, University of Regensburg, 93042 Regensburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nobuhiro","family":"Fujii","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Sapporo Medical University School of Medicine, Chuo-ku, Sapporo 060-8556, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ken-ichi","family":"Amano","sequence":"additional","affiliation":[{"name":"Bioscience Education and Research Center, Akita University, Akita 010-8543, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1209385"},{"key":"e_1_3_2_3_2","first-page":"1941","volume":"54","year":"2007","unstructured":"Asahi, K., H. 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