Refereed journal article or data article (A1)
Preterm infant meconium microbiota transplant induces growth failure, inflammatory activation, and metabolic disturbances in germ-free mice
List of Authors: Hiltunen Henni, Hanani Hila, Luoto Raakel, Turjeman Sondra, Ziv Oren, Isolauri Erika, Salminen Seppo, Koren Omry, Rautava Samuli
Publisher: ELSEVIER
Publication year: 2021
Journal: Cell Reports Medicine
Journal name in source: CELL REPORTS MEDICINE
Journal acronym: CELL REP MED
Article number: ARTN 100447
Volume number: 2
Issue number: 11
Number of pages: 12
ISSN: 2666-3791
eISSN: 2666-3791
DOI: http://dx.doi.org/10.1016/j.xcrm.2021.100447
URL: https://www.sciencedirect.com/science/article/pii/S2666379121003153?via%3Dihub
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/68304874
Preterm birth may result in adverse health outcomes. Very preterm infants typically exhibit postnatal growth restriction, metabolic disturbances, and exaggerated inflammatory responses. We investigated the differences in the meconium microbiota composition between very preterm (<32 weeks), moderately preterm (32-37 weeks), and term (>37 weeks) human neonates by 16S rRNA gene sequencing. Human meconium microbiota transplants to germ-free mice were conducted to investigate whether the meconium microbiota is causally related to the preterm infant phenotype in an experimental model. Our results indicate that very preterm birth is associated with a distinct meconium microbiota composition. Fecal microbiota transplant of very preterm infant meconium results in impaired growth, altered intestinal immune function, and metabolic parameters as compared to term infant meconium transplants in germ-free mice. This finding suggests that measures aiming to minimize the long-term adverse consequences of very preterm birth should be commenced during pregnancy or directly after birth.
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