1. Recent findings have suggested a significant involvement of the immune system in the control of pain. Immune cells contain opioid peptides that are released within inflamed tissue and act at opioid receptors on peripheral sensory nerve endings. It is also apparent that different types of lymphocytes contain beta-endorphin, memory T cells containing more beta-endorphin than naïve cells. 2. These findings highlight an integral link between immune cell migration and inflammatory pain. The present review highlights immune system involvement in the site-directed control of inflammatory pain. 3. Full-length mRNA transcripts for opioid precursor proteins are expressed in immune cells. Increased expression of pro-opiomelanocortin mRNA and beta-endorphin has been demonstrated in stimulated lymphocytes and lymphocytes from animals with inflammation. 4. Cytokines and corticotropin-releasing factor (CRF) release opioids from immune cells. Potent peripheral analgesia due to direct injection of CRF can be blocked by antagonists to CRF, antibodies to opioid peptides, antisense to CRF and opioid receptor-specific antagonists. The release of opioid peptides from lymphocytes is calcium dependent and opioid receptor specific. Furthermore, endogenous sources of opioid peptides produce potent analgesia when implanted into the spinal cord. 5. Activated immune cells migrate directly to inflamed tissue using cell adhesion molecules to adhere to the epithelial surface of the vasculature in inflamed tissue. Lymphocytes that have been activated can express opioid peptides. Memory type T cells that contain opioid peptides are present within inflamed tissue; naive cells are not present in inflamed tissue and do not contain opioid peptides. Inhibiting the migration of memory type T cells into inflamed tissue by blocking selectins results in reduced numbers of beta-endorphin-containing cells, a reduced quantity of beta-endorphin in inflamed paws and reduced stress- and CRF-induced peripheral analgesia. 6. Immunosuppression is associated with increased pain in patients. Moreover, immunosuppression results in decreased lymphocyte numbers as well as decreased analgesia in animal models.

译文

1。最近的发现表明免疫系统在控制疼痛方面有很大的参与。免疫细胞含有阿片肽,这些肽在发炎的组织中释放,并作用于周围感觉神经末梢的阿片受体。同样明显的是,不同类型的淋巴细胞含有 β-内啡肽,记忆T细胞含有比幼稚细胞更多的 β-内啡肽。2.这些发现突出了免疫细胞迁移和炎性疼痛之间不可或缺的联系。本综述强调了免疫系统参与炎性疼痛的定点控制。3.阿片前体蛋白的全长mRNA转录本在免疫细胞中表达。在患有炎症的动物的受刺激的淋巴细胞和淋巴细胞中,已证明了亲黑皮素mRNA和 β-内啡肽的表达增加。4.细胞因子和促肾上腺皮质激素释放因子 (CRF) 从免疫细胞中释放阿片类药物。由于直接注射CRF而产生的有效的外周镇痛作用可被CRF拮抗剂,阿片肽抗体,CRF反义和阿片受体特异性拮抗剂阻断。阿片肽从淋巴细胞的释放是钙依赖性和阿片受体特异性的。此外,当植入脊髓时,阿片肽的内源性来源会产生有效的镇痛作用。5.活化的免疫细胞利用细胞黏附分子直接迁移到发炎组织中,粘附到发炎组织的脉管系统的上皮表面。已经被激活的淋巴细胞可以表达阿片肽。含有阿片肽的记忆型T细胞存在于发炎的组织中; 幼稚细胞不存在于发炎的组织中,也不包含阿片肽。通过阻断选择素来抑制记忆型T细胞向发炎组织的迁移,导致含 β-内啡肽的细胞数量减少,发炎的爪子中 β-内啡肽的数量减少,并减少压力和CRF引起的外周镇痛。6.免疫抑制与患者疼痛增加有关。此外,免疫抑制会导致动物模型中淋巴细胞数量减少以及镇痛作用降低。

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