Neonatal Intensive Care Unit, Royal Victoria Infirmary, Newcastle-upon-Tyne Hospitals (NuTH) NHS Trust, Newcastle, NE2 4BJ, UK.
Translational and Clinical Research Institute, Newcastle University, Framlington Place, Newcastle, NE2 4HH, UK.
Pediatr Res. 2022 Oct;92(4):979-986. doi: 10.1038/s41390-021-01930-8. Epub 2021 Dec 24.
IgA and its secretory form sIgA impact protection from infection and necrotising enterocolitis but little is known about quantities in preterm mums own milk (MOM) or infant stool, onset of endogenous production in the preterm gut, and what affects these.
We measured by ELISA in MOM and stool from healthy preterm infants total IgA and sIgA longitudinally and additionally in MOM fresh, refrigerated, frozen, and after traversing feeding systems.
In 42 MOM (median gestation 26 weeks), we showed total IgA levels and sIgA were highest in colostrum, fell over 3 weeks, and were not impacted by gestation. Median IgA values matched previous term studies (700 mcg/ml). In MOM recipients stool IgA was detected in the first week, at around 30% of MOM quantities. Formula fed infants did not have detectable stool IgA until the third week. Levels of IgA and sIgA were approximately halved by handling processes.
MOM in the 3 weeks after preterm delivery contains the highest concentrations of IgA and sIgA. Endogenous production after preterm birth occurs from the 3 week meaning preterm infants are dependent on MOM for IgA which should be optimised. Routine NICU practices halve the amount available to the infant.
(Secretory) Immunoglobulin A (IgA) is present in colostrum of maternal milk from infants as preterm as 23-24 weeks gestational age, falling over the first 3 weeks to steady levels similar to term. Gestation at birth does not impact (secretory) IgA levels in breast milk. IgA is present in very preterm infant stools from maternal milk fed infants from the first week of life, but not in formula milk fed preterm infants until week three, suggesting endogenous production from this point. Refrigeration, freezing, and feeding via plastic tubing approximately halved the amount of IgA available.
IgA 及其分泌型 sIgA 可预防感染和坏死性小肠结肠炎，但人们对早产儿母乳（MOM）或婴儿粪便中的 IgA 量、早产儿肠道内内源性产生的起始时间以及哪些因素会影响 IgA 量知之甚少。
我们通过 ELISA 法对健康早产儿的 MOM 和粪便中的总 IgA 和 sIgA 进行了纵向测量，此外还对 MOM 的新鲜、冷藏、冷冻以及通过喂养系统后的样本进行了测量。
在 42 例 MOM（中位孕龄 26 周）中，我们发现初乳中的总 IgA 和 sIgA 水平最高，在 3 周内下降，且不受孕龄影响。MOM 受者粪便中的 IgA 可在第 1 周检测到，约为 MOM 量的 30%。配方奶喂养的婴儿直到第 3 周才检测到粪便中的 IgA。处理过程会使 IgA 和 sIgA 的水平降低约一半。
早产儿出生后 3 周内的 MOM 中含有最高浓度的 IgA 和 sIgA。早产儿出生后内源性产生 IgA 的时间为第 3 周，这意味着早产儿依赖 MOM 中的 IgA，应优化 MOM 中的 IgA 水平。NICU 的常规操作会使婴儿可获得的 IgA 量减少一半。
（分泌型）免疫球蛋白 A（IgA）存在于 23-24 周胎龄早产儿的初乳中，在最初的 3 周内下降，达到与足月相似的稳定水平。出生时的孕龄不会影响母乳中的（分泌型）IgA 水平。从生命的第一周开始，从母乳中喂养的非常早产儿的粪便中就存在 IgA，但从配方奶中喂养的早产儿直到第 3 周才存在 IgA，这表明从此时开始内源性产生 IgA。冷藏、冷冻和通过塑料管喂养会使 IgA 的量减少约一半。
