Chemokines CCL2 and CCL7, but not CCL12, play a significant role in the development of pain-related behavior and opioid-induced analgesia

Kwiatkowski, Klaudia; Popiołek-Barczyk, Katarzyna; Piotrowska, Anna; Rojewska, Ewelina; Ciapała, Katarzyna; Makuch, Wioletta; Mika, Joanna

doi:10.1016/j.cyto.2019.03.007

Cited by 45 publications

(91 citation statements)

References 59 publications

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“…CCR1 appears to be important for pain processing, as many CC chemokines that act via this receptor have pronociceptive properties. It has been shown that injection of CCL2, CCL3, CCL4, CCL7 and CCL9 may lead to the development of pain‐like behavior in naive animals . Here, we demonstrated that chronic constriction injury led to an increase in the mRNA levels of the majority of CCR1 ligands at different time‐points.…”

Section: Discussionmentioning

confidence: 54%

“…Moreover, there is evidence that chemokines are involved in opioid analgesic efficacy. Recent studies have demonstrated that single administration of CCL2, CCL3, CCL7 and CCL9 neutralizing antibodies can intensify the effectiveness of morphine and/or buprenorphine . These results demonstrate that chemokine systems are involved in opioid signaling and that chemokine receptor blockade may intensify the analgesic effects of opioids.…”

Section: Discussionmentioning

confidence: 85%

“…. CCR1 seems to be a very important receptor because it is a target of several chemokines [CC motif chemokine ligand 2 (CCL2), CCL3, CCL4, CCL5, CCL6, CCL7 and CCL9], which have been suggested to be involved in the pathogenesis of neuropathic pain . There is some evidence demonstrating that CCR1 is involved in nociception.…”

Section: Introductionmentioning

confidence: 99%

“…injection of a CCR1 antagonist (J113863) as well as the neutralization of CCL3 and CCL9 reduces symptoms of diabetic neuropathic pain . Furthermore, our latest data demonstrated that neutralization of two CCR1 endogenous ligands (CCL2 and CCL7) strongly attenuated CCI‐induced neuropathic pain and significantly affected opioid effectiveness, highlighting the role of CCL2 and CCL7 in the pathogenesis of neuropathic pain . Because of the pleiotropic nature of the chemokines, their ability to activate many receptors, as well as the activation of CCR1 by many different chemokines, we wanted to confront previous results and assess which pharmacological manipulation (receptor blockade or ligand neutralization) may be more important in reducing symptoms of neuropathic pain and modulation of nociceptive factors.…”

Section: Introductionmentioning

confidence: 99%

“…CCR1 seems to be a very important receptor because it is a target of several chemokines [CC motif chemokine ligand 2 (CCL2), CCL3, CCL4, CCL5, CCL6, CCL7 and CCL9], 4,[23][24][25][26][27] which have been suggested to be involved in the pathogenesis of neuropathic pain. [28][29][30] There is some evidence demonstrating that CCR1 is involved in nociception. First, Kiguchi et al 31 showed that the up-regulation of CCR1/CCL3 is associated with the development of pain-related symptoms in a model of murine partial sciatic nerve ligation.…”

Section: Introductionmentioning

confidence: 99%

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The blockade of CC chemokine receptor type 1 influences the level of nociceptive factors and enhances opioid analgesic potency in a rat model of neuropathic pain

et al. 2020

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Summary A growing body of evidence has indicated that the release of nociceptive factors, such as interleukins and chemokines, by activated immune and glial cells has crucial significance for neuropathic pain generation and maintenance. Moreover, changes in the production of nociceptive immune factors are associated with low opioid efficacy in the treatment of neuropathy. Recently, it has been suggested that CC chemokine receptor type 1 (CCR1) signaling is important for nociception. Our study provides evidence that the development of hypersensitivity in rats following chronic constriction injury (CCI) of the sciatic nerve is associated with significant up‐regulation of endogenous CCR1 ligands, namely, CCL2, CCL3, CCL4, CCL6, CCL7 and CCL9 in the spinal cord and CCL2, CCL6, CCL7 and CCL9 in dorsal root ganglia (DRG). We showed that single and repeated intrathecal administration of J113863 (an antagonist of CCR1) attenuated mechanical and thermal hypersensitivity. Moreover, repeated administration of a CCR1 antagonist enhanced the analgesic properties of morphine and buprenorphine after CCI. Simultaneously, repeated administration of J113863 reduced the protein levels of IBA‐1 in the spinal cord and MPO and CD4 in the DRG and, as a consequence, the level of pronociceptive factors, such as interleukin‐1β (IL‐1β), IL‐6 and IL‐18. The data obtained provide evidence that CCR1 blockade reduces hypersensitivity and increases opioid‐induced analgesia through the modulation of neuroimmune interactions.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%