CCL5 and cytokine expression in the rat brain: differential modulation by chronic morphine and morphine withdrawal.
CCL5 and cytokine expression in the rat brain: differential modulation by chronic morphine and morphine withdrawal.
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DOI：
10.1016/j.bbi.2013.08.006
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发表时间：
2013-11
影响因子：
15.1
通讯作者：
Mocchetti, Italo
中科院分区：
文献类型：
--
作者：
Campbell, Lee A.;Avdoshina, Valeriya;Rozzi, Summer;Mocchetti, Italo
阿片类药物已被证明会影响免疫系统，并促进中枢神经系统中促炎细胞因子的表达。然而，最近的数据表明，阿片受体的激活增加了体外星形胶质细胞中神经保护性趋化因子CCL 5的表达和释放。为了进一步确定CCL 5与阿片类药物引起的炎症反应之间的相互作用，我们研究了慢性吗啡和吗啡戒断对CCL 5以及促炎细胞因子白细胞介素-1 β（IL-1β）和肿瘤坏死因子-α（TNF-α）体内表达的影响。接受慢性吗啡范例（10 mg/kg增加到30 mg/kg，每天两次，持续5天）的大鼠显示皮质和纹状体内的CCL 5蛋白和mRNA增加了两倍。IL-1β和TNF-α水平无变化。纳洛酮可阻断吗啡的作用。与盐水处理的动物相比，没有递增剂量（10 mg/kg，每天两次）的慢性吗啡范例没有改变CCL 5水平。相反，大鼠自发吗啡戒断表现出较低水平的皮质内的CCL 5，以及增加的水平的促炎细胞因子和Iba-1阳性细胞比盐水处理的大鼠。总之，这些数据表明，吗啡戒断可能会促进细胞因子和其他炎症反应，有可能加剧神经元损伤。
Opioids have been shown to influence the immune system and to promote the expression of pro-inflammatory cytokines in the central nervous system. However, recent data have shown that activation of opioid receptors increases the expression and release of the neuroprotective chemokine CCL5 from astrocytes in vitro. To further define the interaction between CCL5 and inflammation in response to opioids, we have examined the effect of chronic morphine and morphine withdrawal on the in vivo expression of CCL5 as well as of pro-inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Rats undergoing a chronic morphine paradigm (10 mg/kg increasing to 30 mg/kg, twice a day for 5 days) showed a two-fold increase of CCL5 protein and mRNA within the cortex and striatum. No changes were observed in the levels of IL-1β and TNF-α. Naltrexone blocked the effect of morphine. A chronic morphine paradigm with no escalating doses (10 mg/kg, twice a day) did not alter CCL5 levels compared to saline-treated animals. On the contrary, rats undergoing spontaneous morphine withdrawal exhibited lower levels of CCL5 within the cortex as well as increased levels of pro-inflammatory cytokines and Iba-1 positive cells than saline-treated rats. Overall, these data suggest that morphine withdrawal may promote cytokines and other inflammatory responses that have the potential of exacerbating neuronal damage.
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影响因子：
6.2
作者：
El-Hage, Nazira;Bruce-Keller, Annadora J.;Knapp, Pamela E.;Hauser, Kurt F.
通讯作者：
Hauser, Kurt F.
影响因子：
15.1
作者：
Hutchinson, Mark R.;Zhang, Yingning;Shridhar, Mitesh;Evans, John H.;Buchanan, Madison M.;Zhao, Tina X.;Slivka, Peter F.;Coats, Benjamen D.;Rezvani, Niloofar;Wieseler, Julie;Hughes, Travis S.;Landgraf, Kyle E.;Chan, Stefanie;Fong, Stephanie;Phipps, Simon;Falke, Joseph J.;Leinwand, Leslie A.;Maier, Steven F.;Yin, Hang;Rice, Kenner C.;Watkins, Linda R.
通讯作者：
Watkins, Linda R.
影响因子：
56.9
作者：
COCCHI, F;DEVICO, AL;LUSSO, P
通讯作者：
LUSSO, P
影响因子：
4.7
作者：
Desjardins, Stephane;Belkai, Emilie;Marie-Claire, Cynthia
通讯作者：
Marie-Claire, Cynthia
影响因子：
21.3
作者：
Bakhiet, M;Tjernlund, A;Andersson, J
通讯作者：
Andersson, J