2011
DOI: 10.1213/ane.0b013e3182025b15
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Abstract: The present study demonstrates that etanercept restores the antinociceptive effect of morphine in morphine-tolerant rats by inhibition of proinflammatory cytokine TNF-α, IL-1β, and IL-6 expression and spinal neuroinflammation. The results suggest that etanercept could also be an adjuvant therapy for morphine tolerance, which extends the effectiveness of opioids in clinical pain management.

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Cited by 81 publications
(61 citation statements)
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“…IL-1␤ is elevated by morphine (Johnston et al, 2004;Bokhari et al, 2009;Cao et al, 2010), in a ceramide synthase- , sphingosine kinase- (Muscoli et al, 2010), MEK-, and CGRP- ) dependent manner; this effect could be blocked by ibudilast (Hutchinson et al, 2009a), propentofylline (Raghavendra et al, 2004a), and amitriptyline (Tai et al, 2006;Tai et al, 2009), as well as by the blockade of TNF-␣ (etanercept) (Shen et al, 2011). IL-6 elevation after morphine (Johnston et al, 2004;Dave and Khalili, 2010) is dependent on sphingosine kinase (Muscoli et al, 2010), p38, CGRP , and TLR2 and could also be blocked by etanercept (Shen et al, 2011), naltrexone (Bokhari et al, 2009), amitriptyline (Tai et al, 2006;Tai et al, 2009), and propentofylline (Raghavendra et al, 2004a). Finally, morphine elevation of TNF-␣ (Johnston et al, 2004) is dependent on TLR2 , ceramide synthase ), p38, and CGRP ) and is sensitive to amitriptyline (Tai et al, 2006;Tai et al, 2009), naltrexone (Bokhari et al, 2009), naloxone, and ␤-funaltrexamine (Sawaya et al, 2009).…”
Section: Opioid-induced Changes In Non-neuronal Cells Contribute To Tmentioning
confidence: 99%
See 1 more Smart Citation
“…IL-1␤ is elevated by morphine (Johnston et al, 2004;Bokhari et al, 2009;Cao et al, 2010), in a ceramide synthase- , sphingosine kinase- (Muscoli et al, 2010), MEK-, and CGRP- ) dependent manner; this effect could be blocked by ibudilast (Hutchinson et al, 2009a), propentofylline (Raghavendra et al, 2004a), and amitriptyline (Tai et al, 2006;Tai et al, 2009), as well as by the blockade of TNF-␣ (etanercept) (Shen et al, 2011). IL-6 elevation after morphine (Johnston et al, 2004;Dave and Khalili, 2010) is dependent on sphingosine kinase (Muscoli et al, 2010), p38, CGRP , and TLR2 and could also be blocked by etanercept (Shen et al, 2011), naltrexone (Bokhari et al, 2009), amitriptyline (Tai et al, 2006;Tai et al, 2009), and propentofylline (Raghavendra et al, 2004a). Finally, morphine elevation of TNF-␣ (Johnston et al, 2004) is dependent on TLR2 , ceramide synthase ), p38, and CGRP ) and is sensitive to amitriptyline (Tai et al, 2006;Tai et al, 2009), naltrexone (Bokhari et al, 2009), naloxone, and ␤-funaltrexamine (Sawaya et al, 2009).…”
Section: Opioid-induced Changes In Non-neuronal Cells Contribute To Tmentioning
confidence: 99%
“…It is clear from the preclinical literature than opioid tolerance involves several aspects of central immune signaling, because tolerance can be prevented, attenuated, and/or reversed by blockade of the action or formation of the proinflammatory cytokines IL-1␤, TNF-␣, and/or IL-6 (Raghavendra et al, 2002;Shavit et al, 2005a;Hutchinson et al, 2008a;Shen et al, 2011) or chemokines such as CX3CL1 (Johnston et al, 2004); inhibition of MEK activity (and hence blockade of ERK activation) ; selective reductions in microglial p38 or JNK NEUROIMMUNOPHARMACOLOGIC IMPLICATIONS FOR OPIOID ANALGESIA activation (Guo et al, 2009); decreased P2X4 (Horvath et al, 2010b) or P2X7 signaling (Zhou et al, 2010); reduced ceramide/sphingosine signaling Muscoli et al, 2010); inhibition of matrix metalloproteinase 9 (Liu et al, 2010b); nitric oxide and related superoxide protein damage (Muscoli et al, 2007;Batinić-Haberle et al, 2009); or by general anti-inflammatory treatments such as IL-10 (Johnston et al, 2004), fluorocitrate (Song and Zhao, 2001), minocycline (Mika et al, 2007;Cui et al, 2008;Mika et al, 2009), pentoxifylline (Mika et al, 2007), propentofylline (Raghavendra et al, 2003b;Raghavendra et al, 2004a), ibudilast (Ledeboer et al, 2006a;Lilius et al, 2009), and, interestingly, also by ultra-low-dose naloxone, which acts via elevations of IL-10 expression (Lin et al, 2010b). It is noteworthy that blockade of TLR4 using (ϩ)-naloxone also attenuates the development of morphine tolerance, suggesting that one of the initiating triggers of opioid tolerance is direct activation of TLR4 signaling by opioids (Hutchinson et al, 2010c).…”
Section: What Is the Impact Of Proinflammatory Central Immune Signmentioning
confidence: 99%
“…Glia, especially astrocytes which showed long term activation after morphine challenge, could release proinflammatory cytokines such as tumor necrosis factor ␣ (TNF ␣ ) and interleukin 1 ␤ (IL-1 ␤ ) to attenuate morphine analgesia [4,5]. Furthermore, inhibiting glia or neutralizing cytokines could alleviate morphine tolerance [6][7][8][9][10].…”
Section: Introductionmentioning
confidence: 99%
“…In addition, neuroimmune activation and neuroinflammation occur following chronic usage of opioids, which are considered to play important roles in the induction of tolerance and dependence (DeLeo et al, 2004;Shen et al, 2011).…”
Section: Introductionmentioning
confidence: 99%