title: Cloning of Mongolian gerbil cDNAs encoding inflammatory proteins, and their expression in glandular stomach during H. pylori infection.
abstract: Mongolian gerbils are considered to be a good animal model for understanding the development of Helicobacter pylori-associated diseases. However, limitations regarding the genetic information available for this animal species hamper the elucidation of underlying mechanisms. Thus, we have focused on identifying the nucleotide sequences of cDNAs encoding Mongolian gerbil inflammatory proteins, such as interleukin-1 (IL-1beta), tumor necrosis factor alpha (TNF-alpha), cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). Furthermore, we examined the mRNA expression of these genes in the glandular stomach by RT-PCR at 1-8 weeks after H. pylori infection. The deduced amino acid homologies to mouse, rat and human proteins were 86.2%, 83.6% and 67.8% for IL-1beta, 87.2%, 85.1% and 78.4% for TNF-alpha , 91.9%, 90.2% and 84.8% for COX-2 and 90.8%, 89.1% and 80.1% for iNOS, respectively. The average stomach weight of Mongolian gerbils inoculated with H. pylori was increased in a time-dependent manner at 1, 2, 4 and 8 weeks after inoculation. In the pyloric region, mRNA expression levels of IL-1beta, TNF-alpha and iNOS were increased in H. pylori-infected animals at the 2 weeks time point, while in the fundic region, expression levels of IL-1beta, TNF-alpha and iNOS were elevated at 4 and 8 weeks. The COX-2 expression level in the fundic region was clearly elevated in infected animals compared with control animals at 4 and 8 weeks, but in the pyloric region, expression levels were similar in both infected and control animals. Thus, our results indicate that oxidative stress occurs from an early stage of H. pylori infection in the glandular stomach of Mongolian gerbils.
authors.affiliation: Cancer Prevention Basic Research Project, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Matsubara
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Shibata
authors.forename: Mami
authors.initials: M
authors.lastname: Takahashi
authors.forename: Fumiyasu
authors.initials: F
authors.lastname: Ishikawa
authors.forename: Teruo
authors.initials: T
authors.lastname: Yokokura
authors.forename: Takashi
authors.initials: T
authors.lastname: Sugimura
authors.forename: Keiji
authors.initials: K
authors.lastname: Wakabayashi
mesh_terms: D000818:Animals; D003001:Cloning, Molecular; D051546:Cyclooxygenase 2; D018076:DNA, Complementary; D005753:Gastric Mucosa / Q000378:metabolism*; D005756:Gastritis / Q000378:metabolism / Q000382:microbiology; D005849:Gerbillinae; D016481:Helicobacter Infections / Q000235:genetics / Q000378:metabolism* / Q000382:microbiology; D016480:Helicobacter pylori / Q000302:isolation & purification; D007375:Interleukin-1 / Q000378:metabolism; D053583:Interleukin-1beta; D007527:Isoenzymes / Q000378:metabolism*; D019402:Macrophage Inflammatory Proteins / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II; D009929:Organ Size; D010446:Peptide Fragments / Q000378:metabolism; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D013270:Stomach / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018076:DNA, Complementary; D007375:Interleukin-1; D053583:Interleukin-1beta; D007527:Isoenzymes; D019402:Macrophage Inflammatory Proteins; D010446:Peptide Fragments; D014409:Tumor Necrosis Factor-alpha; C052994:interleukin-1beta (163-171); D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases