Enteric glial cells in the enteric nervous system are critical for the regulation of gastrointestinal homeostasis. Increasing evidence suggests two-way communication between enteric glial cells and both enteric neurons and immune cells. These interactions may be important in the pathogenesis of Crohn's disease (CD), a chronic relapsing disease characterized by a dysregulated immune response. Structural abnormalities in glial cells have been identified in CD. Furthermore, classical inflammatory pathways associated with CD (e.g., the nuclear factor kappa-B pathway) function in enteric glial cells. However, the specific mechanisms by which enteric glial cells contribute to CD have not been summarized in detail. In this review, we describe the possible roles of enteric glial cells in the pathogenesis of CD, including the roles of glia-immune interactions, neuronal modulation, neural plasticity, and barrier integrity. Additionally, the implications for the development of therapeutic strategies for CD based on enteric glial cell-mediated pathogenic processes are discussed.
Keyphrases
- induced apoptosis
- cell cycle arrest
- immune response
- nuclear factor
- neuropathic pain
- endoplasmic reticulum stress
- oxidative stress
- cell death
- multiple sclerosis
- rheumatoid arthritis
- toll like receptor
- signaling pathway
- risk assessment
- blood brain barrier
- bone marrow
- cell proliferation
- inflammatory response
- climate change
- nk cells
- drug induced