Contemporary views on inflammatory pain mechanisms: TRPing over innate and microglial pathways [version 1; referees: 3 approved]
Tissue injury, whether by trauma, surgical intervention, metabolic dysfunction, ischemia, or infection, evokes a complex cellular response (inflammation) that is associated with painful hyperalgesic states. Although in the acute stages it is necessary for protective reflexes and wound healing, infla...
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| Format: | Article |
| Language: | English |
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F1000 Research Ltd
2016-09-01
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| Series: | F1000Research |
| Subjects: | |
| Online Access: | http://f1000research.com/articles/5-2425/v1 |
| _version_ | 1819127596287262720 |
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| author | Zhonghui Guan Judith Hellman Mark Schumacher |
| author_facet | Zhonghui Guan Judith Hellman Mark Schumacher |
| author_sort | Zhonghui Guan |
| collection | DOAJ |
| description | Tissue injury, whether by trauma, surgical intervention, metabolic dysfunction, ischemia, or infection, evokes a complex cellular response (inflammation) that is associated with painful hyperalgesic states. Although in the acute stages it is necessary for protective reflexes and wound healing, inflammation may persist well beyond the need for tissue repair or survival. Prolonged inflammation may well represent the greatest challenge mammalian organisms face, as it can lead to chronic painful conditions, organ dysfunction, morbidity, and death. The complexity of the inflammatory response reflects not only the inciting event (infection, trauma, surgery, cancer, or autoimmune) but also the involvement of heterogeneous cell types including neuronal (primary afferents, sensory ganglion, and spinal cord), non-neuronal (endothelial, keratinocytes, epithelial, and fibroblasts), and immune cells. In this commentary, we will examine 1.) the expression and regulation of two members of the transient receptor potential family in primary afferent nociceptors and their activation/regulation by products of inflammation, 2.) the role of innate immune pathways that drive inflammation, and 3.) the central nervous system’s response to injury with a focus on the activation of spinal microglia driving painful hyperalgesic states. |
| first_indexed | 2024-12-22T08:14:26Z |
| format | Article |
| id | doaj.art-06cb57f782b346858d99d2dd3de32a5f |
| institution | Directory Open Access Journal |
| issn | 2046-1402 |
| language | English |
| last_indexed | 2024-12-22T08:14:26Z |
| publishDate | 2016-09-01 |
| publisher | F1000 Research Ltd |
| record_format | Article |
| series | F1000Research |
| spelling | doaj.art-06cb57f782b346858d99d2dd3de32a5f2022-12-21T18:32:56ZengF1000 Research LtdF1000Research2046-14022016-09-01510.12688/f1000research.8710.19372Contemporary views on inflammatory pain mechanisms: TRPing over innate and microglial pathways [version 1; referees: 3 approved]Zhonghui Guan0Judith Hellman1Mark Schumacher2Department of Anesthesia and Perioperative Care, University of California, San Francisco, CA, USADepartment of Anesthesia and Perioperative Care, University of California, San Francisco, CA, USADepartment of Anesthesia and Perioperative Care, University of California, San Francisco, CA, USATissue injury, whether by trauma, surgical intervention, metabolic dysfunction, ischemia, or infection, evokes a complex cellular response (inflammation) that is associated with painful hyperalgesic states. Although in the acute stages it is necessary for protective reflexes and wound healing, inflammation may persist well beyond the need for tissue repair or survival. Prolonged inflammation may well represent the greatest challenge mammalian organisms face, as it can lead to chronic painful conditions, organ dysfunction, morbidity, and death. The complexity of the inflammatory response reflects not only the inciting event (infection, trauma, surgery, cancer, or autoimmune) but also the involvement of heterogeneous cell types including neuronal (primary afferents, sensory ganglion, and spinal cord), non-neuronal (endothelial, keratinocytes, epithelial, and fibroblasts), and immune cells. In this commentary, we will examine 1.) the expression and regulation of two members of the transient receptor potential family in primary afferent nociceptors and their activation/regulation by products of inflammation, 2.) the role of innate immune pathways that drive inflammation, and 3.) the central nervous system’s response to injury with a focus on the activation of spinal microglia driving painful hyperalgesic states.http://f1000research.com/articles/5-2425/v1Immune ResponseInnate ImmunityLeukocyte Signaling & Gene ExpressionMolecular PharmacologyNeurobiology of Disease & RegenerationNeuronal & Glial Cell BiologyNeuronal Signaling MechanismsNeuropharmacology & PsychopharmacologySensory Systems |
| spellingShingle | Zhonghui Guan Judith Hellman Mark Schumacher Contemporary views on inflammatory pain mechanisms: TRPing over innate and microglial pathways [version 1; referees: 3 approved] F1000Research Immune Response Innate Immunity Leukocyte Signaling & Gene Expression Molecular Pharmacology Neurobiology of Disease & Regeneration Neuronal & Glial Cell Biology Neuronal Signaling Mechanisms Neuropharmacology & Psychopharmacology Sensory Systems |
| title | Contemporary views on inflammatory pain mechanisms: TRPing over innate and microglial pathways [version 1; referees: 3 approved] |
| title_full | Contemporary views on inflammatory pain mechanisms: TRPing over innate and microglial pathways [version 1; referees: 3 approved] |
| title_fullStr | Contemporary views on inflammatory pain mechanisms: TRPing over innate and microglial pathways [version 1; referees: 3 approved] |
| title_full_unstemmed | Contemporary views on inflammatory pain mechanisms: TRPing over innate and microglial pathways [version 1; referees: 3 approved] |
| title_short | Contemporary views on inflammatory pain mechanisms: TRPing over innate and microglial pathways [version 1; referees: 3 approved] |
| title_sort | contemporary views on inflammatory pain mechanisms trping over innate and microglial pathways version 1 referees 3 approved |
| topic | Immune Response Innate Immunity Leukocyte Signaling & Gene Expression Molecular Pharmacology Neurobiology of Disease & Regeneration Neuronal & Glial Cell Biology Neuronal Signaling Mechanisms Neuropharmacology & Psychopharmacology Sensory Systems |
| url | http://f1000research.com/articles/5-2425/v1 |
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