Pathological pain and the neuroimmune interface
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TLDR
The current understanding of the contribution of central immune mechanisms to pathological pain is discussed, and how the heterogeneous immune functions of different cells in the CNS could be harnessed to develop new therapeutics for pain control is discussed.Abstract:
Reciprocal signalling between immunocompetent cells in the central nervous system (CNS) has emerged as a key phenomenon underpinning pathological and chronic pain mechanisms Neuronal excitability can be powerfully enhanced both by classical neurotransmitters derived from neurons, and by immune mediators released from CNS-resident microglia and astrocytes, and from infiltrating cells such as T cells In this Review, we discuss the current understanding of the contribution of central immune mechanisms to pathological pain, and how the heterogeneous immune functions of different cells in the CNS could be harnessed to develop new therapeutics for pain control Given the prevalence of chronic pain and the incomplete efficacy of current drugs — which focus on suppressing aberrant neuronal activity — new strategies to manipulate neuroimmune pain transmission hold considerable promiseread more
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Journal ArticleDOI
Different immune cells mediate mechanical pain hypersensitivity in male and female mice
Robert E. Sorge,Josiane C.S. Mapplebeck,Sarah F. Rosen,Simon Beggs,Sarah Taves,Jessica K. Alexander,Loren J. Martin,Jean-Sebastien Austin,Susana G. Sotocinal,Di Chen,Mu Yang,Xiang Qun Shi,Hao Huang,Nicolas J. Pillon,Philip J. Bilan,Yu Shan Tu,Amira Klip,Ru-Rong Ji,Ji Zhang,Michael W. Salter,Jeffrey S. Mogil +20 more
TL;DR: It is found that microglia are not required for mechanical pain hypersensitivity in female mice; female mice achieved similar levels of pain hypers sensitivity using adaptive immune cells, likely T lymphocytes, suggesting that male mice cannot be used as proxies for females in pain research.
Journal ArticleDOI
Pain regulation by non-neuronal cells and inflammation.
TL;DR: This work reviews how non-neuronal cells interact with nociceptive neurons by secreting neuroactive signaling molecules that modulate pain and discusses new therapeutic strategies to control neuroinflammation for the prevention and treatment of chronic pain.
Journal ArticleDOI
Emerging targets in neuroinflammation-driven chronic pain
TL;DR: This Review focuses on emerging targets — such as chemokines, proteases and the WNT pathway — that promote spinal cord neuro inflammation and chronic pain and highlights the anti-inflammatory and pro-resolution lipid mediators that act on immune cells, glial cells and neurons to resolve neuroinflammation, synaptic plasticity and pain.
Journal ArticleDOI
TFOS DEWS II pain and sensation report
Carlos Belmonte,Jason J. Nichols,Stephanie Cox,James A. Brock,Carolyn G. Begley,David A. Bereiter,Darlene A. Dartt,Anat Galor,Anat Galor,Pedram Hamrah,Jason J. Ivanusic,Deborah S. Jacobs,Nancy A. McNamara,Nancy A. McNamara,Mark I. Rosenblatt,Fiona Stapleton,James S. Wolffsohn +16 more
TL;DR: Pain associated with mechanical, chemical, and thermal heat stimulation of the ocular surface is mediated by trigeminal ganglion neurons, while cold thermoreceptors detect wetness and reflexly maintain basal tear production and blinking rate, thereby evoking dryness sensations and pain.
Journal ArticleDOI
Injured sensory neuron-derived CSF1 induces microglial proliferation and DAP12-dependent pain
Zhonghui Guan,Julia Kuhn,Xidao Wang,Bradley M. Colquitt,Carlos Solorzano,Smitha Vaman,Andrew Guan,Zoe Evans-Reinsch,Joao M. Braz,Marshall Devor,Sherry L. Abboud-Werner,Lewis L. Lanier,Stavros Lomvardas,Allan I. Basbaum +13 more
TL;DR: It is found that peripheral nerve injury induced de novo expression of colony-stimulating factor 1 (CSF1) in injured sensory neurons and the microglial membrane adaptor protein DAP12 was required for both nerve injury– and intrathecal CSF1–induced upregulation of pain-related microglia genes and the ensuing pain, but not formicroglial proliferation.
References
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