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Articles by K Kawa
Total Records ( 2 ) for K Kawa
  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.

  D Iwakiri , L Zhou , M Samanta , M Matsumoto , T Ebihara , T Seya , S Imai , M Fujieda , K Kawa and K. Takada
 

Epstein-Barr virus–encoded small RNA (EBER) is nonpolyadenylated, noncoding RNA that forms stem-loop structure by intermolecular base-pairing, giving rise to double-stranded RNA (dsRNA)–like molecules, and exists abundantly in EBV-infected cells. Here, we report that EBER induces signaling from the Toll-like receptor 3 (TLR3), which is a sensor of viral double-stranded RNA (dsRNA) and induces type I IFN and proinflammatory cytokines. A substantial amount of EBER, which was sufficient to induce signaling from TLR3, was released from EBV-infected cells, and the majority of the released EBER existed as a complex with a cellular EBER-binding protein La, suggesting that EBER was released from the cells by active secretion of La. Sera from patients with infectious mononucleosis (IM), chronic active EBV infection (CAEBV), and EBV-associated hemophagocytic lymphohistiocytosis (EBV-HLH), whose general symptoms are caused by proinflammatory cytokines contained EBER, and addition of RNA purified from the sera into culture medium induced signaling from TLR3 in EBV-transformed lymphocytes and peripheral mononuclear cells. Furthermore, DCs treated with EBER showed mature phenotype and antigen presentation capacity. These findings suggest that EBER, which is released from EBV-infected cells, is responsible for immune activation by EBV, inducing type I IFN and proinflammatory cytokines. EBER-induced activation of innate immunity would account for immunopathologic diseases caused by active EBV infection.

 
 
 
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