Abstract
Allergic diseases often commence early in childhood and persist into adulthood. An early predictor of an infant/childhood allergy is the infant gut microbiome, which is consistently shaped by the intake of human milk. While numerous studies have reported associations between the infant gut microbiota and allergy outcomes, studies on human milk microbiota are sparse. Here, we explored associations between the human milk microbiota and infant/child allergic sensitisation and diseases. Full-length 16S rRNA gene sequencing was performed on milk samples collected at 3 months post-partum (n = 232) from the Infant Fish Oil Supplementation (IFOS) study. The IFOS cohort consists of infants of allergic mothers, 32.9% of whom went on to develop allergic disease before 3 years of age. An unpaired t-test was used to compare the differences in the milk microbiome with the child allergy outcomes at 1 and 2–3 years of age. The preliminary results showed no difference in the alpha diversity between the children with and without the allergic disease at 1 and 2–3 years of age. However, the relative abundance of several respiratory bacterial species was different in the milk given to infants with and without allergen sensitisation (p = 0.003–0.041): Streptococcus pneumoniae was less abundant in the milk fed to infants with allergen sensitisation at 1 year (p = 0.041) and at 2–3 years of age (p = 0.019), whereas Pseudomonas sp. was more abundant in the milk fed to infants with allergen sensitisation at 1 year (p = 0.003), but not at 2–3 years of age (p = 0.066). The preliminary analysis identified associations between specific bacteria in human milk and infant/child allergen sensitisation, which require further investigation.
Author Contributions
Conceptualization, D.J.P., L.F.S. and D.T.G.; Writing—original draft preparation, J.M.; writing—review and editing, L.F.S., D.T.G., D.J.P.; experiment and data analysis, J.M.; supervision, L.F.S., D.T.G., D.J.P., C.T.L. All authors have read and agreed to the published version of the manuscript.
Funding
J.M., L.F.S., C.T.L., and D.T.G. are supported by an unrestricted research grant from Medela AG, administered by The University of Western Australia. J.M. was supported by an additional SIRF (Scholarships for International Research Fees) scholarship from The University of Western Australia and Ad Hoc Postgraduate Scholarship from Medela AG.
Institutional Review Board Statement
Not applicable.
Informed Consent Statement
Not applicable.
Data Availability Statement
Data sharing not applicable.
Conflicts of Interest
J.M., L.F.S., C.T.L., and D.T.G. are supported by an unrestricted research grant from Medela AG, administered by The University of Western Australia. This funding body had no input into manuscript design, data interpretation, or decision to publish.
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