@article{oai:hirosaki.repo.nii.ac.jp:00003625,
 author = {Sashinami, Hiroshi and Kageyama, Kazunori and Suda, Toshihiro and Nakane, Akio},
 issue = {Supplement},
 journal = {弘前医学},
 month = {Nov},
 note = {application/pdf, It is well known that corticotropin releasing factor （CRF） modulates immune response duringinfl ammation. We investigated the eff ect of CRF family peptides on host resistance to Listeria monocytogenes infectionin mice. The numbers of L. monoctyogenes in the organs of Ucn2-treated mice were dramatically increased comparedwith CRF- or Ucn-treated mice. CRF receptor type 2 is involved in the suppressive eff ect of Ucn2 on L. monocytogenesinfection. Interferon （IFN）-γ and tumor necrosis factor （TNF）-α production were decreased and interleukin （IL）-10 production was signifi cantly increased in the spleens of Ucn2-treated mice compared with those in Ucn2-untreatedcontrol mice. The eff ect of Ucn2 was canceled by depleting endogenous IL-10 using anti-IL-10 monoclonal antibodyand in IL-10 deficient mice. The expression and activation of signal transducers and activators of transcription3 （STAT3） were up-regulated and the expression and activation of STAT1 were down-regulated in the spleensfrom Ucn2-treated mice compared with vehicle-treated mice. Moreover, suppression of TNF-α production andaugmentation of IL-10 production and expression and activation of STAT3 by Ucn2 treatment were observed in heatkilledL. monocytogenes-stimulated macrophages. These results suggested that Urn2 suppresses host resistance to L.monocytogenes infection via up-regulation of IL-10 production., 弘前医学. 59(Suppl.), 2007, p.S67-S76},
 pages = {S67--S76},
 title = {Urocortin 2 suppresses host resistance to Listeria monocytogenes infection via up-regulation of IL-10},
 volume = {59},
 year = {2007}
}