Recent findings on how proinflammatory cytokines cause pain: peripheral mechanisms in inflammatory and neuropathic hyperalgesia.
By C. Sommer, M. Kress. Neuroscience Letters, 2004
851 citations recorded by the source corpus.
Subfields: Behavioral Neuroscience, Cellular and Molecular Neuroscience, Physiology
View Paper: https://www.semanticscholar.org/paper/d8e1c556a7164fcdd09dcf40c4fa110cf9a8c984
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In Cellular and Molecular Neuroscience
In Physiology
- R. Ji
- M. Malcangio
- Bharat B. Aggarwal
- Clifford J. Woolf
- Alban Latremoliere
- G. Moalem-Taylor
- P. Austin
Citations in the corpus
- Cytokine Mechanisms of Central Sensitization: Distinct and Overlapping Role of Interleukin-1β, Interleukin-6, and Tumor Necrosis Factor-α in Regulating Synaptic and Neuronal Activity in the Superficial Spinal Cord (2008, background): “The proinflammatory cytokines (PICs) such as interleukin-1 (IL1 ), interleukin-6 (IL-6), and tumor necrosis factor- (TNF ) are an important group of inflammatory mediators and play an essential role in pain sensitization (Sorkin et al., 1997; Woolf et al., 1997; Sommer and Kress, 2004).”
- Curcumin and cancer: an "old-age" disease with an "age-old" solution. (2008, background): “Various chemotherapeutic drugs including vincristine, taxanes, and cisplatin have been associated with neuropathic pain [243,244].”
- The neurobiology of itch (2006, background): “The crosstalk between immune cells and neurons has been in the focus of pain research during recent year”
- The role of glia in the spinal cord in neuropathic and inflammatory pain. (2015, background): “Within the CNS IL-1β is expressed at low levels by both neurons and glial cells (Ren and Torres 2009; Clark et al. 2006; Copray et al. 2001; Guo et al. 2007; Sommer and Kress 2004), and the expression of IL-1R1 is equally widespread within the spinal cord (Zhang et al.”
- The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, neutral): “However, there is also strong evidence for direct receptor-mediated effects of some cytokines on nociceptors (Sommer and Kress, 2004).”