Abstract
Globally, it is estimated that one in five people suffer from chronic pain, with prevalence increasing with age. The pathophysiology of chronic pain encompasses complex sensory, immune, and inflammatory interactions within both the central and peripheral nervous systems. Microglia, the resident macrophages of the central nervous system (CNS), are critically involved in the initiation and persistence of chronic pain. Microglia respond to local signals from the CNS but are also modulated by signals from the gastrointestinal tract. Emerging data from preclinical and clinical studies suggest that communication between the gut microbiome, the community of bacteria residing within the gut, and microglia is involved in producing chronic pain. Targeted strategies that manipulate or restore the gut microbiome have been shown to reduce microglial activation and alleviate symptoms associated with inflammation. These data indicate that manipulations of the gut microbiome in chronic pain patients might be a viable strategy in improving pain outcomes. Herein, we discuss the evidence for a connection between microglia and the gut microbiome and explore the mechanisms by which commensal bacteria might influence microglial reactivity to drive chronic pain.
Highlights
The transition from acute to chronic pain is defined by numerous adaptations along the entire neural axis
While injured or degenerating afferents are clearly involved in driving the inflammatory response to injury in the central nervous system (CNS) (Coull et al, 2005; Guan et al, 2015), emerging evidence suggests that the gut microbiome might contribute to the proinflammatory processes that drive chronic pain
Given the clear connection between the gut microbiome and CNS inflammation, it is possible that perturbations within the community of commensal bacteria contribute to a pathogenic microglial phenotype and facilitate the initiation and maintenance of chronic pain
Summary
The transition from acute to chronic pain is defined by numerous adaptations along the entire neural axis. While injured or degenerating afferents are clearly involved in driving the inflammatory response to injury in the central nervous system (CNS) (Coull et al, 2005; Guan et al, 2015), emerging evidence suggests that the gut microbiome might contribute to the proinflammatory processes that drive chronic pain. A relationship between chronic pain and the gut microbiome is becoming increasingly clear. Given the clear connection between the gut microbiome and CNS inflammation, it is possible that perturbations within the community of commensal bacteria contribute to a pathogenic microglial phenotype and facilitate the initiation and maintenance of chronic pain. This review will discuss the complex relationship between the gut microbiome and microglia and explore how intestinal dysbiosis might drive chronic pain through promoting microglial activation
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