Abstract
Preterm infants acquire reduced amounts of Immunoglobulin G (IgG) via trans-placental transfer as compared to term infants which might explain their high susceptibility for infections. The reduced amount of IgG antibodies also results in a lower amount of anti-inflammatory Fc N-galactosylated and -sialylated IgG antibodies. This reduction or, even more, a qualitative shift in the type of IgG Fc glycosylation might contribute to the increased risk for sustained inflammatory diseases in preterm infants. It was the aim of our explorative study to investigate the IgG Fc glycosylation patterns in preterm infants of different gestational ages compared to term infants and mothers of preterm infants. In plasma samples of preterm infants (n = 38), we investigated IgG concentrations by use of ELISA. Furthermore, we analyzed IgG Fc glycosylation patterns in plasma of preterm infants (n = 86, 23–34 weeks of gestation), term infants (n = 15) and mothers from preterm infants (n = 41) using high performance liquid chromatography. Extremely low gestational age infants (born < 28 weeks of gestation during second trimester) had reduced IgG concentrations and decreased proportions of galactosylated (84.5 vs. 88.4%), sialylated (14.5 vs. 17.9%) and bisecting N-acetylglucosamine-containing (8.4 vs. 10.8%) IgG Fc N-linked glycans as compared to preterm infants born ≥28 weeks of gestation (during third trimester) and term infants. Increased non-galactosylated (agalactosylated, 16.9 vs. 10.6%) IgG Fc N-linked glycans were associated with the development of chronic inflammatory bronchopulmonary dysplasia (BPD). However, mothers of preterm infants born during second or third trimester of pregnancy did not show significant differences in IgG Fc glycosylation patterns. Thus, the IgG Fc glycosylation patterns of preterm infants depend on their gestational age. Although lack of bisecting N-acetylglucosamine has been associated with less inflammatory effector functions, the decreased IgG Fc galactosylation and sialylation with lower gestational age suggest a rather pro-inflammatory pattern. The difference in IgG Fc glycosylation patterns between preterm infants and mothers of preterm infants suggests a selective enrichment of IgG glyco forms in preterm infants, which might contribute to or result of the development of sustained inflammatory diseases like BPD.
Highlights
The adaptation of women during pregnancy leads to a fetomaternal immune tolerance, which is disrupted in the settings of preterm birth
To analyze whether plasma Immunoglobulin G (IgG) concentrations and Fc glycosylation patterns differ with gestational age, we divided the cohort in 2 gestational age groups (center 1/center 2: ≥23(+0 days) and ≤27(+6) weeks, n = 19/n = 43; ≥28(+0) and ≤34(+6) weeks, n = 19/n = 43; Tables 1, 2)
We noted that IgG Fc glycosylation patterns of preterm infants differ with gestational age whereas the patterns of mothers, as described in the literature [32, 33], did not differ with gestational age of their offspring
Summary
The adaptation of women during pregnancy leads to a fetomaternal immune tolerance, which is disrupted in the settings of preterm birth. Reasons for preterm birth are often associated with rather pro-inflammatory conditions at the feto-maternal interface (e.g., infection, age, stress) [1]. Specific immune protection of infants against pathogens is provided by the active transport of IgG through the placenta probably exclusively via the neonatal Fc receptor (FcRn) [6,7,8,9,10]. During week 17–22 of gestation only 5–10% of maternal IgG concentrations are transported via the placenta, which rises to 50% during week 28–32 of gestation [11]. Reduced IgG concentrations in preterm infants might contribute to their predisposition for infection [9]
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