Commensal microbiota is fundamental for the development of inflammatory pain
Commensal microbiota is fundamental for the development of inflammatory pain
复制标题
DOI：
10.1073/pnas.0711891105
复制
发表时间：
2008-02-12
影响因子：
11.1
通讯作者：
Teixeira, M. M.
中科院分区：
文献类型：
--
作者：
Amaral, F. A.;Sachs, D.;Teixeira, M. M.
个人感觉疼痛的能力是其适应环境和避免损害的能力的基础。急性或慢性炎症可增强痛感。在目前的研究中，我们调查了炎性疼痛是否在没有微生物区系的情况下被修改，这是通过过敏性伤害反应来衡量的。为此，我们评估了一系列炎症刺激在无菌小鼠和常规小鼠中诱导的机械性伤害性反应。我们的实验表明，在无菌小鼠中，角叉菜胶、脂多糖、肿瘤坏死因子-α、白介素1-β和趋化因子CXCL1诱导的炎性高伤害性感觉减少。相比之下，前列腺素和多巴胺在无菌小鼠或常规小鼠中诱导的过敏性伤害感相似。卡拉胶诱导的高度伤害性感觉的减少与组织炎症的减少有关，并且可以通过微生物区系的重新定位或全身注射脂多糖来逆转。值得注意的是，在无菌小鼠中，过度伤害性感受的减少伴随着刺激后IL-10表达的增加，并可以通过抗IL-10抗体的治疗而逆转。因此，这些结果表明，接触共生微生物区系对于小鼠发展炎性过敏性伤害性感觉是必要的。这些发现暗示了共生微生物区系和宿主之间的相互作用在促进对环境压力的适应方面发挥了重要作用，包括那些引起疼痛的环境压力。
The ability of an individual to sense pain is fundamental for its capacity to adapt to its environment and to avoid damage. The sensation of pain can be enhanced by acute or chronic inflammation. In the present study, we have investigated whether inflammatory pain, as measured by hypernociceptive responses, was modified in the absence of the microbiota. To this end, we evaluated mechanical nociceptive responses induced by a range of inflammatory stimuli in germ-free and conventional mice. Our experiments show that inflammatory hypernociception induced by carrageenan, lipopolysaccharide, TNF-alpha, IL-1 beta, and the chemokine CXCL1 was reduced in germfree mice. In contrast, hypernociception induced by prostaglandins and dopamine was similar in germ-free or conventional mice. Reduction of hypernociception induced by carrageenan was associated with reduced tissue inflammation and could be reversed by reposition of the microbiota or systemic administration of lipopolysaccharide. Significantly, decreased hypernociception in germ-free mice was accompanied by enhanced IL-10 expression upon stimulation and could be reversed by treatment with an anti-IL-10 antibody. Therefore, these results show that contact with commensal microbiota is necessary for mice to develop inflammatory hypernociception. These findings implicate an important role of the interaction between the commensal microbiota and the host in favoring adaptation to environmental stresses, including those that cause pain.