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Nature:抑制新生儿免疫系统可促进其肠道益生菌生长

  1. 免疫系统
  2. 新生儿
  3. 肠道益生菌

来源:科学网 2013-11-14 15:20

据《自然》期刊发表的一项研究显示,抑制新生儿免疫系统可确保其益生菌在肠道内蓬勃发展。

据《自然》期刊发表的一项研究显示,抑制新生儿免疫系统可确保其益生菌在肠道内蓬勃发展。活鼠和人脐血样本实验挑战传统观念,证明免疫系统发育不完全不是导致新生儿在出生后头几个星期免疫功能低下的原因。研究结果有助于开展医疗策略,改善新生儿的免疫力。

美国俄亥俄州辛辛那提儿童医院医疗中心Sing Sing Way教授与其科研团队证明表达CD71受体的红血细胞(CD71+细胞)能抑制6日龄小鼠的免疫反应。他们也发现人脐血中CD71+细胞具有独特的免疫抑制特性,但成年小鼠的CD71+细胞却没有这些特性,这结果表明免疫抑制特性只限于新生儿。研究人员指出,新生儿的免疫系统虽然被抑制,但其益生菌的生长能被改善,而益生菌对此关键发育时期尤其重要。他们表明,抑制免疫力的CD71+细胞能防止小鼠肠道建立起益生菌群是过度发炎。

因此,新生儿的免疫低下可能是其肠道菌群发展的‘副产品’。(生物谷Bioon.com)

生物谷推荐的英文摘要

Nature      doi:10.1038/nature12675

Immunosuppressive CD71+ erythroid cells compromise neonatal host defence against infection

Shokrollah Elahi,James M. Ertelt,Jeremy M. Kinder,Tony T. Jiang,Xuzhe Zhang,Lijun Xin,Vandana Chaturvedi,Beverly S. Strong,Joseph E. Qualls,Kris A. Steinbrecher,Theodosia A. Kalfa,Aimen F. Shaaban& Sing Sing Way

Newborn infants are highly susceptible to infection. This defect in host defence has generally been ascribed to the immaturity of neonatal immune cells; however, the degree of hyporesponsiveness is highly variable and depends on the stimulation conditions1, 2, 3, 4, 5, 6, 7. These discordant responses illustrate the need for a more unified explanation for why immunity is compromised in neonates. Here we show that physiologically enriched CD71+ erythroid cells in neonatal mice and human cord blood have distinctive immunosuppressive properties. The production of innate immune protective cytokines by adult cells is diminished after transfer to neonatal mice or after co-culture with neonatal splenocytes. Neonatal CD71+ cells express the enzyme arginase-2, and arginase activity is essential for the immunosuppressive properties of these cells because molecular inhibition of this enzyme or supplementation with l-arginine overrides immunosuppression. In addition, the ablation of CD71+ cells in neonatal mice, or the decline in number of these cells as postnatal development progresses parallels the loss of suppression, and restored resistance to the perinatal pathogens Listeria monocytogenes and Escherichia coli8, 9. However, CD71+ cell-mediated susceptibility to infection is counterbalanced by CD71+ cell-mediated protection against aberrant immune cell activation in the intestine, where colonization with commensal microorganisms occurs swiftly after parturition10, 11. Conversely, circumventing such colonization by using antimicrobials or gnotobiotic germ-free mice overrides these protective benefits. Thus, CD71+ cells quench the excessive inflammation induced by abrupt colonization with commensal microorganisms after parturition. This finding challenges the idea that the susceptibility of neonates to infection reflects immune-cell-intrinsic defects and instead highlights processes that are developmentally more essential and inadvertently mitigate innate immune protection. We anticipate that these results will spark renewed investigation into the need for immunosuppression in neonates, as well as improved strategies for augmenting host defence in this vulnerable population.

 

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