Abstract
Pain is a signal of inflammation that can be both protective and
pathogenic. Macrophages, a significant component of the immune system,
play an essential role in the occurrence and development of pain,
particularly in neuroimmune communication. Macrophages exhibit two
distinct phenotypes: pro-inflammatory M1-like and anti-inflammatory
M2-like phenotypes. Sensory neurons can promote macrophages into the M1
phenotype to produce pro-inflammatory mediators to defend against
infection while causing tissue damage and inducing pain. However, this
can be inhibited by M2 macrophages, facilitated by sensory nerves,
resulting in pain resolution. This article provides an overview of the
interplay between sensory nerves and M1/M2 macrophages during the
induction and resolution of pain.