Pain in autoimmune disorders

Mifflin, Katherine A.; Kerr, Bradley J.

doi:10.1002/jnr.23844

Cited by 39 publications

(22 citation statements)

References 148 publications

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“…Evidence for the involvement of B cells in the initiation of pain mainly comes from studies that show that autoantibodies can induce pain [ 148 ]. Autoantibodies against citrullinated antigens (ACPAs; e.g.…”

Section: Immune Cells Regulating Painmentioning

confidence: 99%

Divergent roles of immune cells and their mediators in pain

2017

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Chronic pain is a major debilitating condition that is difficult to treat. Although chronic pain may appear to be a disorder of the nervous system, crucial roles for immune cells and their mediators have been identified as important contributors in various types of pain. This review focuses on how the immune system regulates pain and discusses the emerging roles of immune cells in the initiation or maintenance of chronic pain. We highlight which immune cells infiltrate damaged nerves, the dorsal root ganglia, spinal cord and tissues around free nerve endings and discuss through which mechanisms they control pain. Finally we discuss emerging roles of the immune system in resolving pain and how the immune system contributes to the transition from acute to chronic pain. We propose that targeting some of these immune processes may provide novel therapeutic opportunities for the treatment of chronic pain.

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Section: Immune Cells Regulating Painmentioning

confidence: 99%

Divergent roles of immune cells and their mediators in pain

2017

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“…Among them, inflammation holds a crucial role as most brain cells are glia, which have an important role in quickly spreading inflammation [6,7]. More specifically, clustered differentiation of 4+ (CD4+) T lymphocytes produces a subset of cells called T-helper 17 (Th17) cells [8], which act as a pro-inflammatory factor in inflammation [9–11]. Reports have shown that Th17 cells are active participants in PD pathogenesis [8].…”

Section: Introductionmentioning

confidence: 99%

Increased Levels of Pro-Inflammatory and Anti-Inflammatory Cellular Responses in Parkinson’s Disease Patients: Search for a Disease Indicator

Yang¹,

Guo

Zhu³

et al. 2017

Med Sci Monit

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BackgroundParkinson’s disease (PD) is the second most prevalent neurodegenerative disorder and it arises when most of the dopaminergic neurons of substantia nigra region die. Several mechanisms have been postulated as the causative event in PD pathology, and neuroinflammation is most crucial among them.Material/MethodsWe analyzed T-helper 17 (Th17) cells and myeloid-derived suppressor cells (MDSCs) from 80 PD patients to assess inflammatory processes and to find a cost-effective means to evaluate PD prognosis.ResultsWe found significantly increased numbers of Th17 cells and MDSCs count in peripheral circulation in PD patients compared with controls (p<0.001). A positive correlation was found between Th17 cells and MDSCs in PD patients (r=0.421, p<0.05).ConclusionsOur results show the effector role of Th17 cells and MDSCs in PD pathology and shows their utility as effective biomarkers for PD diagnosis.

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“…The role of cytokines in hyperalgesic and inflammatory processes, including arthritis, is well documented [82–84]. The sensitization of nociceptors by cytokines is a multi-mediated process that involves the release of prostaglandins and sympathomimetic amines [68, 69, 72, 85, 86].…”

Section: Discussionmentioning

confidence: 99%

Articular inflammation induced by an enzymatically-inactive Lys49 phospholipase A2: activation of endogenous phospholipases contributes to the pronociceptive effect

Dias

Sampaio

Sant’Anna

et al. 2017

J Venom Anim Toxins Incl Trop Dis

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BackgroundArthritis is a set of inflammatory conditions that induce aching, stiffness, swelling, pain and may cause functional disability with severe consequences to the patient’s lives. These are multi-mediated pathologies that cannot be effectively protected and/or treated. Therefore, the aim of this study was to establish a new model of acute arthritis, using a Lys49-PLA2 (Bothrops asper myotoxin II; MT-II) to induce articular inflammation.MethodsThe articular inflammation was induced by MT-II (10 μg/joint) injection into the left tibio-tarsal or femoral-tibial-patellar joints. Cellular influx was evaluated counting total and differential cells that migrated to the joint. The plasma extravasation was determined using Evans blue dye. The edematogenic response was evaluated measuring the joint thickness using a caliper. The articular hypernociception was determined by a dorsal flexion of the tibio-tarsal joint using an electronic pressure-meter test. The mediators involved in the articular hypernociception were evaluated using receptor antagonists and enzymatic inhibitors.ResultsPlasma extravasation in the knee joints was observed 5 and 15 min after MT-II (10 μg/joint) injection. MT-II also induced a polymorphonuclear cell influx into the femoral-tibial-patellar joints observed 8 h after its injection, a period that coincided with the peak of the hyperalgesic effect. Hyperalgesia was inhibited by the pretreatment of the animals with cyclooxygenase inhibitor indomethacin, with type-2 cyclooxygenase inhibitor celecoxib, with AACOCF3 and PACOCF3, inhibitors of cytosolic and Ca2+-independent PLA2s, respectively, with bradykinin B2 receptor antagonist HOE 140, with antibodies against TNFα, IL-1β, IL-6 and CINC-1 and with selective ET-A (BQ-123) and ET-B (BQ-788) endothelin receptors antagonists. The MT-II-induced hyperalgesia was not altered by the lipoxygenase inhibitor zileuton, by the bradykinin B1 receptor antagonist Lys-(Des-Arg9,Leu8)-bradykinin, by the histamine and serotonin antagonists promethazine and methysergide, respectively, by the nitric oxide inhibitor LNMMA and by the inhibitor of matrix 1-, 2-, 3-, 8- and 9- metalloproteinases GM6001 (Ilomastat).ConclusionThese results demonstrated the multi-mediated characteristic of the articular inflammation induced by MT-II, which demonstrates its relevance as a model for arthritis mechanisms and treatment evaluation.

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Pain in autoimmune disorders

Cited by 39 publications

References 148 publications

Divergent roles of immune cells and their mediators in pain

Divergent roles of immune cells and their mediators in pain

Increased Levels of Pro-Inflammatory and Anti-Inflammatory Cellular Responses in Parkinson’s Disease Patients: Search for a Disease Indicator

Articular inflammation induced by an enzymatically-inactive Lys49 phospholipase A2: activation of endogenous phospholipases contributes to the pronociceptive effect

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