Pattern recognition receptors in chronic pain: Mechanisms and therapeutic implications

Kato, Jungo; Agalave, Nilesh M.; Svensson, Camilla I.

doi:10.1016/j.ejphar.2016.06.039

Cited by 37 publications

(33 citation statements)

References 185 publications

(219 reference statements)

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“…Toll-like receptors (TLR) are activated by endogenous damage-associated molecular patterns (DAMPs) such as fragmented extracellular matrix components, HMGB1 and heat-shock proteins. Many DAMPs are increased in RA models [31,79,87,116] and TLRs are expressed on a number of cell types, including immune cells, glia, chondrocytes, synoviocytes, osteoclasts and sensory neurons [54,79,95].…”

Section: Toll-like Receptorsmentioning

confidence: 99%

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Pain pathogenesis in rheumatoid arthritis—what have we learned from animal models?

Krock

Jurczak²,

Svensson³

2018

Pain

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Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by joint inflammation and joint pain. Much of RA treatment is focused on suppressing inflammation, with the idea being that if inflammation is controlled other symptoms, such as pain, will disappear. However, pain is the most common complaint of RA patients, is often still present following the resolution of inflammation, and can develop prior to the onset of inflammation. Thus, further research is needed to better understand RA-associated pain mechanisms. A number of preclinical rodent models commonly used in rheumatology research have been developed based on bedside-to-bench and reverse translational approaches. These models include collagen-induced arthritis, antigen-induced arthritis, streptococcal

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Section: Toll-like Receptorsmentioning

confidence: 99%

“…TLR signaling increases nociceptive factors, such TNF and nerve growth factor [79,93], and joint inflammation in RA models [79,124]. In male K/BxN mice, spinal gene expression of the TLR4 ligands tenascin-c and HSP90 are increased [31] and extranuclear HMGB1 increases in male and female CAIA mice [3].…”

Section: Toll-like Receptorsmentioning

confidence: 99%

Pain pathogenesis in rheumatoid arthritis—what have we learned from animal models?

Krock

Jurczak²,

Svensson³

2018

Pain

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“…Pain is an undesired feeling that can produce a wide range of responses: from mild, localized ache to distress [1][2][3]. Despite its displeasure, it is one of the vital body alarm systems, as it allows the subject to recognize stimuli of potentially harmful intensities [4]. Pain may be located on a specific area, such as an injury, but it can also be more diffuse, as it occurs with many diseases [3].…”

Section: Introductionmentioning

confidence: 99%

“…In contrast to short-lasting acute pain, chronic pain persists even after the cessation of the initial cause and often loses its protective value [1,4,6]. By definition, chronic pain lasts over 3-6 months [7] and is not solved with treatment [8].…”

Section: Introductionmentioning

confidence: 99%

“…Its origin may be nociceptive or neuropathic [7,9], and it can be triggered by various causes (chronic musculoskeletal pain [10,11], chronic low back pain [12], fibromyalgia [13], tension-type headache [14], osteoarthritis [15], whiplash [16], heart and respiratory systems [7,17], endometriosis [18], etc.). Once developed, it may become resistant to standard treatments, greatly affecting patient quality of life [4].…”

Section: Introductionmentioning

confidence: 99%

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Sensor Technologies to Manage the Physiological Traits of Chronic Pain: A Review

Naranjo-Hernández

Reina‐Tosina

Roa

2020

Sensors

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Non-oncologic chronic pain is a common high-morbidity impairment worldwide and acknowledged as a condition with significant incidence on quality of life. Pain intensity is largely perceived as a subjective experience, what makes challenging its objective measurement. However, the physiological traces of pain make possible its correlation with vital signs, such as heart rate variability, skin conductance, electromyogram, etc., or health performance metrics derived from daily activity monitoring or facial expressions, which can be acquired with diverse sensor technologies and multisensory approaches. As the assessment and management of pain are essential issues for a wide range of clinical disorders and treatments, this paper reviews different sensor-based approaches applied to the objective evaluation of non-oncological chronic pain. The space of available technologies and resources aimed at pain assessment represent a diversified set of alternatives that can be exploited to address the multidimensional nature of pain.

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Antinociceptive activity of the novel RAGE inhibitor, papaverine, in a mouse model of chronic inflammatory pain

Yoshizawa

Takeuchi

Nakamura

et al. 2020

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It has been recognized that a chronic pain state involves sensory neuronal excitability enhanced by pro-inflammatory cytokines or other inflammatory mediators secreted from immune cells (Grace et al., 2014). Many researchers have attempted to interfere with this mechanism as a novel therapeutic approach. High-mobility group box 1 (HMGB1), released from damaged necrotic cells or activated immune cells, is an essential nuclear protein for gene transcriptional modulation or DNA structural support (Agalave & Svensson, 2015). The variation in receptors for HMGB1 makes it difficult to target its signaling. Extracellular HMGB1 mediates the inflammatory response through the activation of pattern recognition receptors, including the receptor for advanced glycation end products (RAGE) and toll-like receptors (TLRs) (van Beijnum et al., 2008). Furthermore, HMGB1 mediates the release of inflammatory cytokines, such as interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and interferons from microglia (Agalave & Svensson, 2015). These signaling pathways are involved in pathological conditions, such as sepsis, rheumatoid arthritis, cancer, ischemia, and

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Pattern recognition receptors in chronic pain: Mechanisms and therapeutic implications

Cited by 37 publications

References 185 publications

Pain pathogenesis in rheumatoid arthritis—what have we learned from animal models?

Pain pathogenesis in rheumatoid arthritis—what have we learned from animal models?

Sensor Technologies to Manage the Physiological Traits of Chronic Pain: A Review

Antinociceptive activity of the novel RAGE inhibitor, papaverine, in a mouse model of chronic inflammatory pain

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