Mycoplasma hyopneumoniae induces pro-inflammatory cytokine and nitric oxide production through NF kappa B and MAPK pathways in RAW264.7 cells
文献类型: 外文期刊
作者: Hwang, Mi-Hyun 1 ; Damte, Dereje 1 ; Lee, Joong-Su 1 ; Gebru, Elias 1 ; Chang, Zhi-Qiang 1 ; Cheng, Henrique 2 ; Jung, 1 ;
作者机构: 1.Kyungpook Natl Univ, Coll Vet Med, Taegu 702701, South Korea
2.Louisiana State Univ, Sch Vet Med, Baton Rouge, LA 70803 USA
3.Natl Vet Res & Quarantine Serv, Anyang 430824, South Korea
4.Chinese Acad Fishery Sci, Yellow Sea Fisheries Res Inst, Qingdao 266071, Peoples R China
关键词: Mycoplasma hyopneumoniae;MAPK;NF-kappa B;RAW264.7 cells
期刊名称:VETERINARY RESEARCH COMMUNICATIONS ( 影响因子:2.459; 五年影响因子:2.352 )
ISSN: 0165-7380
年卷期: 2011 年 35 卷 1 期
页码:
收录情况: SCI
摘要: In the present study, we confirmed the ability of M. hyopneumoniae to induce the secretion of large amount of proinflammatory cytokine and nitric oxide (NO) in murine macrophage RAW 264.7 cells. Moreover, M. hyopneumoniae-induced activation of the MAPK and NF-kappa B pathways by phosphorylation of ERK1/2, p38 and JNK/SAPK and by dissociation of I kappa B from NF-kappa B. Translocation of transcription factor NF-kappa B and its binding was confirmed through western blot and electromobility shift assay. From these results, we further hypothesized that these signal proteins were involved in M. hyopneumoniae-induced proinflammatory cytokines and NO productions in macrophages. Hence, we utilized specific blockers of MAPK and NF-kappa B to investigate the signaling pathway involvement in cytokine and NO production through pharmacological approaches. The results demonstrated significant inhibition of TNF-alpha, IL-1 beta, IL-6 and NO by MAPK inhibitors. NF-kappa B inhibitor PDTC significantly inhibited IL-1 beta and NO production. These findings contribute to the understanding of the mechanisms of immune reactivity and may ultimately prove useful in the development of new therapeutic strategies. In summary, we found critical evidence for the involvement of NF-kappa B and MAPK signaling pathways in the upregulation of proinflammatory cytokine and NO induced by M. hyopneumoniae.
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