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Articles by Y Iwakura
Total Records ( 2 ) for Y Iwakura
  K Kawa , H Tsutsui , R Uchiyama , J Kato , K Matsui , Y Iwakura , T Matsumoto and K. Nakanishi
 

Hyper-coagulation, hypothermia, systemic inflammatory responses and shock are major clinical manifestations of endotoxin shock syndrome in human. As previously reported, mice primed with heat-killed Propionibacterium acnes are highly susceptible to the action of LPS to induce tumour necrosis factor (TNF)- and to that of TNF- to trigger lethal shock. Here we investigated the mechanisms underlying the P. acnes-induced sensitization to LPS and TNF- and the development of individual symptoms after subsequent challenge with LPS or TNF-. Propionibacterium acnes-primed wild-type (WT) mice, but not naive mice, exhibited hyper-coagulation with elevated levels of thrombin–antithrombin complexes and anti-fibrinolytic plasminogen activator inhibitor 1 in their plasma, hypothermia, systemic inflammatory responses and high mortality rate after LPS or TNF- challenge. Propionibacterium acnes treatment reportedly induces both Th1 and Th17 cell development. Propionibacterium acnes-primed Il12p40–/– and Ifn–/– mice, while not Il17A–/– mice, evaded all these symptoms/signs upon LPS or TNF- challenge, indicating essential requirement of IL-12–IFN- axis for the sensitization to LPS and TNF-. Furthermore, IFN- blockade just before LPS challenge could prevent P. acnes-primed WT mice from endotoxin shock syndrome. These results demonstrated requirement of IFN- to the development of endotoxin shock and suggested it as a potent therapeutic target for the treatment of septic shock.

  M Munoz , M. M Heimesaat , K Danker , D Struck , U Lohmann , R Plickert , S Bereswill , A Fischer , I. R Dunay , K Wolk , C Loddenkemper , H. W Krell , C Libert , L. R Lund , O Frey , C Holscher , Y Iwakura , N Ghilardi , W Ouyang , T Kamradt , R Sabat and O. Liesenfeld
 

Peroral infection with Toxoplasma gondii leads to the development of small intestinal inflammation dependent on Th1 cytokines. The role of Th17 cells in ileitis is unknown. We report interleukin (IL)-23–mediated gelatinase A (matrixmetalloproteinase [MMP]-2) up-regulation in the ileum of infected mice. MMP-2 deficiency as well as therapeutic or prophylactic selective gelatinase blockage protected mice from the development of T. gondii–induced immunopathology. Moreover, IL-23–dependent up-regulation of IL-22 was essential for the development of ileitis, whereas IL-17 was down-regulated and dispensable. CD4+ T cells were the main source of IL-22 in the small intestinal lamina propria. Thus, IL-23 regulates small intestinal inflammation via IL-22 but independent of IL-17. Gelatinases may be useful targets for treatment of intestinal inflammation.

 
 
 
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