Abstract
Bidirectional interactions between the immune system and the nervous system are increasingly appreciated as playing a pathogenic role in chronic pain. Unraveling the mechanisms by which inflammatory pain is mediated through communication between nerves and immune cells may lead to exciting new strategies for therapeutic intervention. In this narrative review, we focus on the role of macrophages in the pathogenesis of osteoarthritis (OA) pain. From regulating homeostasis to conducting phagocytosis, and from inducing inflammation to resolving it, macrophages are plastic cells that are highly adaptable to their environment. They rely on communicating with the environment through cytokines, growth factors, neuropeptides, and other signals to respond to inflammation or injury. The contribution of macrophages to OA joint damage has garnered much attention in recent years. Here, we discuss how macrophages may participate in the initiation and maintenance of pain in OA. We aim to summarize what is currently known about macrophages in OA pain and identify important gaps in the field to fuel future investigations.
Original language | English (US) |
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Pages (from-to) | E892 |
Journal | Pain Reports |
Volume | 6 |
Issue number | 1 |
DOIs | |
State | Published - Jan 9 2021 |
Funding
The authors are grateful for the support of the National Institutes of Health (National Institute of Arthritis and Musculoskeletal and Skin Diseases [NIAMS]) (grant numbers K01AR070328 to R.E. Miller, R01AR060364 and R61AR073576 to A.-M. Malfait, R01AR064251 to A.-M. Malfait and R.J. Miller, T32AR073157 to T. Geraghty). A.-M. Malfait is supported by the George W. Stuppy, MD, Chair of Arthritis at Rush University.
Keywords
- Animal models
- Inflammation
- Macrophages
- Neuroimmunity
- Osteoarthritis
- Pain
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine