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1 First Department of Surgery, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
2 Division of Gene Therapy Science, Osaka University, Graduate School of Medicine, Suita, Osaka, Japan
3 Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
4 Department of Pathology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
5 Department of Immunology and Medical Zoology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
* To whom correspondence should be addressed. E-mail: surg-1{at}hyo-med.ac.jp.
Hepatocyte growth factor (HGF), a multifunctional cytokine, accelerates intestinal
epithelial proliferation. We studied effects of HGF in mice with trinitrobenzene sulfonic
acid (TNBS)-induced colitis, which shows clinical and molecular resemblance to Crohn's
disease. Mice with colitis repeatedly were transfected intramuscularly with human HGF
cDNA. Weight, survival, histopathology, pro-inflammatory cytokine mRNAs, and
leukocyte infiltration were assessed. Treatment with HGF cDNA induced tyrosine
phosphorylation of intestinal c-Met/HGF receptors, inhibited apoptosis, and promoted
mitosis in intestinal epithelial cells, accelerating intestinal epithelial restoration and
suppressing inflammation. Transfection with HGF cDNA markedly suppressed intestinal
mRNA expression of Th1 cytokines such as interleukin (IL)-12, and -1
, interferon-
, and
tumor necrosis factor-
. Numbers of total and CD4-positive T cells, neutrophils, and
myloperoxidase activity in intestinal epithelium were diminished by HGF gene transfer,
which also prevented weight loss and improved survival. HGF might prove useful for
controlling inflammatory bowel disease.
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