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JNK and NF-κB pathways mediate the production of IL-1β, IL-6 and TNF-α under induction of the rL-hemolysins for 24 h.

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posted on 20.02.2013, 01:32 by Huan Wang, Yifei Wu, David M. Ojcius, X. Frank Yang, Chenglin Zhang, Shibiao Ding, Xu’ai Lin, Jie Yan

Bars show the mean ± SD of three independent experiments. E-LPS indicates the LPS of E. coli serotype O111:B4. PK-H indicates that the rL-hemolysins or E-LPS were pretreated with proteinase K digestion plus heat-inactivation while PMB indicates that the rL-hemolysins or E-LPS were pretreated with polymyxin B blockade, and were used to monitor possible contamination with E. coli LPS in the rL-hemolysin proteins. The concentration of each of the rL-hemolysins or E-LPS tesed was 1 µg. Control indicates the IL-1β, IL-6 and TNF-α levels in the human THP-1 and mouse J774A.1 macrophages before treatment with any rL-hemolysins or E-LPS. #P<0.05 vs IL-1β, IL-6 and TNF-α levels in the THP-1 or J774A.1 macrophages before treatment with any rL-hemolysins or E-LPS (control). *P<0.05 vs IL-1β, IL-6 and TNF-α levels in the THP-1 or J774A.1 macrophages that had not been treated with different signaling pathway inhibitors (SN50 for the NF-κB pathway, SP600125 for the JNK pathway, and SB203580 for the p38MAPK pathway).

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