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Updated: Feb 19, 2026
A Murine Model of Group B Streptococcus Vaginal Colonization
Published on: November 16, 2016
SIgA, TGF-β1, IL-10, and TNFα in Colostrum Are Associated with Infant Group B Streptococcus Colonization
Kirsty Le Doare1,2,3,1, Katie Bellis2, Amadou Faal3
1Imperial College London, London, United Kingdom.
Insights
High levels of secretory IgA (SIgA) and cytokines in breast milk may protect infants from Group B Streptococcus (GBS) colonization. Maternal breast milk factors appear crucial for preventing infant GBS disease.
Area of Science:
- Immunology
- Neonatal Health
- Microbiology
Background:
- Group B Streptococcus (GBS) is a significant cause of infant mortality and morbidity.
- Maternal colonization is a primary transmission route, yet most infants remain unaffected.
- The role of breast milk immune factors in infant GBS colonization and protection is unclear.
Purpose of the Study:
- To examine the link between breast milk secretory IgA (SIgA) and cytokines and infant GBS colonization and clearance.
- To identify specific immune factors in breast milk associated with protection against GBS.
Main Methods:
- Prospective cohort study of 750 Gambian mother/infant pairs up to 89 days postpartum.
- Assessed anti-GBS SIgA by flow cytometry and quantified 12 cytokines in breast milk and serum.
- Determined mother/infant GBS colonization status.
Main Results:
- Higher anti-GBS SIgA in colostrum correlated with reduced GBS colonization risk for serotypes III and V.
- Infants with GBS colonization at day 6 received colostrum with higher levels of TGF-β1, TNFα, IL10, and IL-6.
- Elevated colostral TGF-β1, TNFα, and IL-6 enhanced GBS clearance between birth and day 89.
Conclusions:
- Increased anti-GBS SIgA in breast milk may decrease infant GBS colonization risk.
- Maternal cytokines in breast milk may offer protection against infant GBS colonization.
- Findings support developing interventions, such as maternal vaccination, to reduce infant GBS colonization.
Background:
Group B Streptococcus (GBS) is a major cause of mortality and morbidity in infants and is associated with transmission from a colonized mother at birth and via infected breastmilk. Although maternal/infant colonization with GBS is common, the majority of infants exposed to GBS remain unaffected. The association between breastmilk immune factors and infant colonization and disease prevention has not been elucidated.
Objectives:
We have investigated the association between SIgA and cytokines in breastmilk and infant GBS colonization and clearance.
Methods:
Mother/infant GBS colonization was determined in a prospective cohort of 750 Gambian mother/infant pairs followed to day 89 of life. Anti-GBS secretory IgA bound to the surface of whole bacteria was assessed by flow cytometry and a panel of 12 cytokines quantified by mesoscale discovery in colostrum, breastmilk and serum.
Results:
Compared with infants receiving low anti-GBS SIgA in colostrum, infants receiving high anti-GBS SIgA were at decreased risk of GBS colonization for serotypes III and V. Infants colonized at day 6 were twice as likely to receive colostrum with high TGF-β1, TNFα, IL10, and IL-6 compared to uncolonized infants. Infants receiving high colostral TGF-β1, TNFα, and IL-6 had two-fold enhanced GBS clearance between birth and day 89.
Conclusion:
Our results suggest that the infant GBS colonization risk diminishes with increasing anti-GBS SIgA antibody in breastmilk and that key maternally derived cytokines might contribute to protection against infant colonization. These findings might be leveraged to develop interventions including maternal vaccination that may reduce infant GBS colonization.
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