The role of the M1/M2 microglia in the process from cancer pain to morphine tolerance

Cancer pain, especially bone cancer pain, is a pain state often caused by inflammation or dysfunctional nerves. Moreover, in the management of cancer pain, opioid especially morphine is widely used, however, it also brings severe side effects such as morphine tolerance to the patient (Deandrea et al., 2008). A growing body of literatures demonstrated that neuroinflammation is mediated by microglia. As the macrophages like immune cells, microglia play an important role in the pathogenesis of cancer pain and morphine tolerance. Microglia acquire different activation states to regulate the function of these cells. As to M1 phenotype, microglia release pro-inflammatory cytokines and neurotoxic molecules that promote inflammation and cytotoxic reactions. Conversely, when microglia represent M2 phenotypes secreting anti-inflammatory cytokines and nutrient factors that promote the function of repair, regeneration and restore homeostasis. A better understanding of microglia activation in cancer pain and morphine tolerance is crucial for the development of hypothesized neuroprotective drugs. Targeting microglia different polarization states by the inhibition of their deleterious pro-inflammatory neurotoxicity and/or enhancing their beneficial anti-inflammatory protective function seems to be an effective treatment for cancer pain and morphine tolerance.

Automated summary

Microglia play a crucial role in the pathogenesis of cancer pain and morphine tolerance, as they acquire different activation states to regulate their function. Targeting the activation states of microglia can be an effective treatment for cancer pain and morphine tolerance by inhibiting their harmful pro-inflammatory neurotoxicity and enhancing their beneficial anti-inflammatory protective function.