›› 2016, Vol. 43 ›› Issue (6): 1437-1445.doi: 10.16431/j.cnki.1671-7236.2016.06.006

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Effect of AIR on Inflammatory Reaction Infected by Brucella

XU Ya-fang1, CHEN Chuang-fu1, WANG Hao1, FU Qiang2, SHI Hui-jun2, SUN Zhi-hua3, ZHANG Hui1, GUO Fei4   

  1. 1. College of Animal Science and Technology, Shihezi University, Shihezi 832003, China;
    2. College of Veterinary Medicine, Xinjiang Agricultural University, Urumqi 830000, China;
    3. Key Laboratory for Tropical Biological Resources, Ministry of Education, Hainan University, Haikou 570228, China;
    4. School of Medicine, Shihezi University, Shihezi 832002, China
  • Received:2015-10-08 Online:2016-06-20 Published:2016-07-11

Abstract: In order to investigate the effect of AIR on inflammatory reaction infected by Brucellamelitensis (16M), the AIR domain of Tecpr1 gene of murine macrophages RAW264.7 were knocked down (I-A), overexpressed (O-A) and reversed (OA-IA). Using the chlorine fluorescein (DCFH-DA) as a probe, we detected the variation of ROS production and mitochondria distribution by confocal laser scanning microscopy. We observed the expression changes of NLRP3, ASC and Caspase-1 by qRT-PCR and the expression changes of IL-18,IL-1β and Caspase-1 in host cells by ELISA. The results showed that 16M could stimulate RAW264.7 cells to produce ROS by time-dependent pathway, and I-A group and O-A group showed more abnormal accumulation of mitochondrial. The results of qRT-PCR and ELISA suggested that it had effect on the expression levels of NLRP3, ASC,Caspase-1 and IL-18, IL-1β and Caspase-1 in cells of different groups. Those results indicated that with AIR gene deletion, the release amount of ROS changed, mitochondrial clustered abnormally, and AIR was closely related to the activation of inflammasomes and induction of inflammatory reactions.

Key words: Brucella; AIR; ROS; mitochondria; inflammasome

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