Langhendries J-P, Maton P, François A, Marguglio A, Marion W, Smeets S, Philippet P
CHC-Site St Vincent, NICU, Rue François Lefèbvre 207, Liège-Rocourt, Belgique.
Arch Pediatr. 2010 Sep;17 Suppl 3:S110-8. doi: 10.1016/S0929-693X(10)70910-6.
The pre and postnatal development of human immunity are remarkably continuous. The feto-placental unit builds up to promote a climate of immune tolerance specifically driven in this way by the maternal immunity. The process of birth triggers the development of the infant's postnatal immunity, in first place through the bacterial colonisation of a sterile intestinal mucosa. The progressive immune response stabilisation at the sub-mucosa level during the first year of life will arise from the interface between the host and its microflora. It will take place progressively and will occur thanks to a variety of successive and complementary very complex immune mechanisms, under the influence of a rich and diversified intestinal microbiotia. Solid scientific arguments allow hypothesising that immune deviances later in life could be the consequence of an inadequate bacterial pressure on the intestinal mucosa at the early stage. A variety of epigenetic modifications taking place in this early stage could account for the deviant programming of later immunity. Each health care provider should acknowledge that some therapeutic and nutritional interventions during the first year of life may interfere with this complex immune development, giving rise to a risk of increasing immune deviancies later on.
人类免疫的产前和产后发育具有显著的连续性。胎儿 - 胎盘单位逐渐形成,以营造一种由母体免疫以这种特定方式驱动的免疫耐受环境。出生过程触发婴儿产后免疫的发育,首先是通过无菌肠黏膜的细菌定植。在生命的第一年,黏膜下层水平的免疫反应逐渐稳定,这将源于宿主与其微生物群之间的相互作用。这一过程将逐步发生,并且得益于各种连续且互补的非常复杂的免疫机制,在丰富多样的肠道微生物群的影响下实现。有力的科学论据支持这样的假设,即生命后期的免疫偏差可能是早期肠道黏膜上细菌压力不足的结果。在这个早期阶段发生的各种表观遗传修饰可能解释后期免疫的异常编程。每位医疗保健提供者都应认识到,生命第一年的某些治疗和营养干预可能会干扰这种复杂的免疫发育,从而增加后期出现免疫偏差的风险。