周围神经系统(PNS)内的炎症过程与痛觉过敏和异常性疼痛的症状相关。促炎介质,如细胞因子或前列腺素,调节伤害性神经元的兴奋性,称为外周致敏。这里,我们旨在研究先前报道的脂多糖(LPS)体外刺激对背根神经节(DRG)原代细胞培养物的影响是否反映了体内LPS诱导的全身性炎症模型的变化.雄性大鼠腹膜内注射LPS(100μg/kg)或生理盐水。全身性炎症对炎症介质表达的影响,神经元Ca2+反应,并评估DRG中炎性转录因子的激活。全身炎症伴随着腰椎DRG中促炎细胞因子和环氧合酶-2的表达增强。在从LPS处理的大鼠获得的DRG原代培养物中,可以检测到增强的神经元辣椒素反应。此外,我们发现,与生理盐水对照组相比,体内LPS攻击后,培养的巨噬细胞和神经元中炎症转录因子的激活增加.总的来说,我们的研究强调了炎症过程在PNS中的作用,这些炎症过程可能与全身性LPS治疗引起的疾病行为相关痛觉过敏有关.此外,我们提出了DRG原代培养作为在细胞水平上研究炎症过程的工具,不仅在体外,而且在体外。
Inflammatory processes within the peripheral nervous system (PNS) are associated with symptoms of hyperalgesia and allodynia. Pro-inflammatory mediators, such as cytokines or prostaglandins, modulate the excitability of nociceptive neurons, called peripheral sensitization. Here, we aimed to examine if previously reported effects of in vitro stimulation with lipopolysaccharide (LPS) on primary cell cultures of dorsal root ganglia (DRG) reflect changes in a model of LPS-induced systemic inflammation in vivo. Male rats were intraperitoneally injected with LPS (100 µg/kg) or saline. Effects of systemic inflammation on expression of inflammatory mediators, neuronal Ca2+ responses, and activation of inflammatory transcription factors in DRG were assessed. Systemic inflammation was accompanied by an enhanced expression of pro-inflammatory cytokines and cyclooxygenase-2 in lumbar DRG. In DRG primary cultures obtained from LPS-treated rats enhanced neuronal capsaicin-responses were detectable. Moreover, we found an increased activation of inflammatory transcription factors in cultured macrophages and neurons after an in vivo LPS challenge compared to saline controls. Overall, our
study emphasizes the role of inflammatory processes in the PNS that may be involved in sickness-behavior-associated hyperalgesia induced by systemic LPS treatment. Moreover, we present DRG primary cultures as tools to
study inflammatory processes on a cellular level, not only in vitro but also ex vivo.