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.