Mechanisms of inflammatory pain

Kidd, Bruce L.; Urbán, László

doi:10.1093/bja/87.1.3

Cited by 509 publications

(351 citation statements)

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“…Inflammatory pain may result from enhanced nociception due to the interaction of inflammatory mediators with neurons and the resulting state of hypersensitivity. Inflammation may also cause damage to neurons and produce neuropathic pain [34] . Being the largest group of sensory receptors, GPCRs play important roles in inflammatory nociception.…”

Section: Gpcrs and Inflammatory Painmentioning

confidence: 99%

Role of G protein-coupled receptors in inflammation

2012

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Section: Gpcrs and Inflammatory Painmentioning

confidence: 99%

Role of G protein-coupled receptors in inflammation

2012

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“…However, the inflammatory response needs to be controlled with carefully balanced pro-and antiinflammatory elements and clearing of necrotic tissue and elimination of pathogens, promoting tissue repair and a return of tissue homeostasis. Pain is a cardinal feature of inflammation and is often referred to as inflammatory pain when the two symptoms occur together (1). The activation of nociceptive sensory neurons during inflammation serves the important role of alerting the organism to the presence of tissue injury/inflammation, with the associated pain hypersensitivity contributing to the avoidance of further damage until healing has occurred (2).…”

mentioning

confidence: 99%

CD11b⁺Ly6G⁻myeloid cells mediate mechanical inflammatory pain hypersensitivity

Ghasemlou

Chiu

Julien

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

156

135

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Pain hypersensitivity at the site of inflammation as a result of chronic immune diseases, pathogenic infection, and tissue injury is a common medical condition. However, the specific contributions of the innate and adaptive immune system to the generation of pain during inflammation have not been systematically elucidated. We therefore set out to characterize the cellular and molecular immune response in two widely used preclinical models of inflammatory pain: (i) intraplantar injection of complete Freund's adjuvant (CFA) as a model of adjuvant-and pathogen-based inflammation and (ii) a plantar incisional wound as a model of tissue injury-based inflammation. Our findings reveal differences in temporal patterns of immune cell recruitment and activation states, cytokine production, and pain in these two models, with CFA causing a nonresolving granulomatous inflammatory response whereas tissue incision induced resolving immune and pain responses. These findings highlight the significant differences and potential clinical relevance of the incisional wound model compared with the CFA model. By using various cell-depletion strategies, we find that, whereas lymphocyte antigen 6 complex locus G (Ly)6G + CD11b + neutrophils and T-cell receptor (TCR) β + T cells do not contribute to the development of thermal or mechanical pain hypersensitivity in either model, proliferating CD11b + Ly6G − myeloid cells were necessary for mechanical hypersensitivity during incisional pain, and, to a lesser extent, CFA-induced inflammation. However, inflammatory (CCR2 + Ly6C hi ) monocytes were not responsible for these effects. The finding that a population of proliferating CD11b + Ly6G − myeloid cells contribute to mechanical inflammatory pain provides a potential cellular target for its treatment in wound inflammation.pain | inflammation | cytokines | monocytes | macrophages

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“…Previous work examining the role of inflammation in altered sensitivity shows that with profoundly increased inflammation there can be an alteration in both thermal and mechanical sensation (Andrew & Greenspan, 1999; Kidd & Urban, 2001). Examination of painful areas has revealed that mast cells are a key marker of inflammatory changes in pain states and offer a key correlation between their density and resulting sensitivity (Heron & Dubayle, 2013).…”

Section: Discussionmentioning

confidence: 99%

Rats bred for low and high running capacity display alterations in peripheral tissues and nerves relevant to neuropathy and pain

et al. 2017

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IntroductionDiet and activity are recognized as modulators of nervous system disease, including pain. Studies of exercise consistently reveal a benefit on pain. This study focused on female rats to understand differences related to metabolic status and peripheral nerve function in females.MethodsHere, we investigated parameters of peripheral nerve function relevant to pain in rats selectively bred for high (high‐capacity runners; HCR) or low endurance exercise capacity (low‐capacity runners; LCR) resulting in divergent intrinsic aerobic capacities and susceptibility for metabolic conditions.Results LCR female rats have reduced mechanical sensitivity, higher intraepidermal nerve fiber density and TrkA‐positive epidermal axons, increased numbers of Langerhans and mast cells in cutaneous tissues, and a higher fat content despite similar overall body weights compared to female HCR rats. Sensory and motor nerve conduction velocities, thermal sensitivity, and mRNA expression of selected genes relevant to peripheral sensation were not different.ConclusionsThese results suggest that aerobic capacity and metabolic status influence sensory sensitivity and aspects of inflammation in peripheral tissues that could lead to poor responses to tissue damage and painful stimuli. The LCR and HCR rats should prove useful as models to assess how the metabolic status impacts pain.

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Mechanisms of inflammatory pain

Cited by 509 publications

References 73 publications

Role of G protein-coupled receptors in inflammation

Role of G protein-coupled receptors in inflammation

CD11b⁺Ly6G⁻myeloid cells mediate mechanical inflammatory pain hypersensitivity

Rats bred for low and high running capacity display alterations in peripheral tissues and nerves relevant to neuropathy and pain

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Mechanisms of inflammatory pain

Cited by 509 publications

References 73 publications

Role of G protein-coupled receptors in inflammation

Role of G protein-coupled receptors in inflammation

CD11b+Ly6G−myeloid cells mediate mechanical inflammatory pain hypersensitivity

Rats bred for low and high running capacity display alterations in peripheral tissues and nerves relevant to neuropathy and pain

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CD11b⁺Ly6G⁻myeloid cells mediate mechanical inflammatory pain hypersensitivity