Division of Inflammation Medicine, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Am J Reprod Immunol. 2011 Jul;66 Suppl 1:75-80. doi: 10.1111/j.1600-0897.2011.01036.x.
The increasing allergy prevalence in affluent countries may be caused by reduced microbial stimulation, resulting in an abnormal post-natal immune maturation. Most studies investigating the underlying mechanisms have focused on post-natal microbial exposure. Also, the maternal microbial environment during pregnancy may program the immune development of the child, however.
This review focuses on how maternal immunity and microbial exposures regulate childhood immune and allergy development.
Prenatal environmental exposures may alter gene expression via epigenetic mechanisms, aiming to induce physiological adaptations to the anticipated post-natal environment, but potentially also increasing disease susceptibility in the offspring. Although the importance of fetal programming mostly has been studied in cardiovascular and metabolic disease, this hypothesis is also very attractive in the context of environmentally influenced immune-mediated diseases.
Efficacious preventive measures, required to combat the allergy epidemic, may be identified by determining how the immune interaction between mother and child is influenced by microbial factors.
富裕国家过敏发病率的上升可能是由于微生物刺激减少，导致出生后免疫成熟异常。大多数研究潜在机制的研究都集中在后生微生物暴露上。然而，怀孕期间母体的微生物环境也可能影响儿童的免疫发育。
本综述重点探讨了母体免疫和微生物暴露如何调节儿童免疫和过敏发展。
产前环境暴露可以通过表观遗传机制改变基因表达，旨在诱导对预期出生后环境的生理适应，但也可能使后代更容易患病。尽管胎儿编程的重要性主要在心血管和代谢疾病中进行了研究，但在环境影响的免疫介导疾病的背景下，这一假设也非常有吸引力。
通过确定母亲和孩子之间的免疫相互作用如何受到微生物因素的影响，可能确定有效的预防措施来对抗过敏流行。
