Curto-Reyes Verdad, Kirschmann Guylène, Pertin Marie, Drexler Stephan K, Decosterd Isabelle, Suter Marc R
Pain Center, Department of Anesthesiology, Lausanne University Hospital (CHUV) and University of Lausanne, Lausanne, Switzerland; Department of Fundamental Neurosciences, University of Lausanne, Lausanne, Switzerland.
Department of Biochemistry, University of Lausanne, Epalinges, Switzerland.
PLoS One. 2015 Jul 28;10(7):e0133707. doi: 10.1371/journal.pone.0133707. eCollection 2015.
The NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome is one of the main sources of interleukin-1β (IL-1β) and is involved in several inflammatory-related pathologies. To date, its relationship with pain has not been studied in depth. The aim of our study was to elucidate the role of NLRP3 inflammasome and IL-1β production on neuropathic pain. Results showed that basal pain sensitivity is unaltered in NLRP3-/- mice as well as responses to formalin test. Spared nerve injury (SNI) surgery induced the development of mechanical allodynia and thermal hyperalgesia in a similar way in both genotypes and did not modify mRNA levels of the NLRP3 inflammasome components in the spinal cord. Intrathecal lipopolysaccharide (LPS) injection increases apoptosis-associated speck like protein (ASC), caspase-1 and IL-1β expression in both wildtype and NLRP3-/- mice. Those data suggest that NLRP3 is not involved in neuropathic pain and also that other sources of IL-1β are implicated in neuroinflammatory responses induced by LPS.
含NACHT、LRR和PYD结构域蛋白3（NLRP3）炎性小体是白细胞介素-1β（IL-1β）的主要来源之一，参与多种炎症相关疾病。迄今为止，其与疼痛的关系尚未得到深入研究。我们研究的目的是阐明NLRP3炎性小体和IL-1β产生在神经性疼痛中的作用。结果显示，NLRP3基因敲除小鼠的基础疼痛敏感性以及对福尔马林试验的反应未改变。两种基因型的小鼠在备用神经损伤（SNI）手术后均以相似方式诱导了机械性异常性疼痛和热痛觉过敏，且未改变脊髓中NLRP3炎性小体成分的mRNA水平。鞘内注射脂多糖（LPS）可增加野生型和NLRP3基因敲除小鼠中凋亡相关斑点样蛋白（ASC）、半胱天冬酶-1和IL-1β的表达。这些数据表明，NLRP3不参与神经性疼痛，且其他IL-1β来源与LPS诱导的神经炎症反应有关。
