Sepsis, gut bacteria, and breast milk

A substance found in breast milk appears to prevent migration of pathogenic bacteria from the gut to the bloodstream of newborn mice, according to a study. In preterm infants, late-onset sepsis causes one-quarter of all deaths and increases the risk of neurocognitive problems. Using a mouse model, Kathryn Knoop and colleagues found that a substance found in breast milk appears to prevent migration of pathogenic Escherichia coli from the gut to the bloodstream of newborn mice. The authors developed the mouse model to determine the role of epidermal growth factor (EGF), a molecule that is found in high concentrations in colostrum, a form of breast milk, and that decreases over time. The authors disrupted EGF receptor signaling in mouse pups and inoculated the pups with E. coli strains isolated from the gastrointestinal tracts of septic, preterm infants. Pups with the disrupted receptors died, whereas controls, as well as pups inoculated only with commensal species, did not. Examining the pups’ intestines, the authors found that pups with disrupted EGF receptors had developed goblet cell-associated passageways, which are cellular gaps through which bacteria could pass. Subsequently, the authors demonstrated that EGF acts directly on goblet cells and prevents the formation of the passageways. According to the authors, the results suggest that donated breast milk collected closer to the time of birth–when EGF levels are high–is likely to provide increased protection against late-onset sepsis.

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Article #19-12022: “Maternal activation of the EGFR prevents translocation of gut-residing pathogenic Escherichia coli in a model of late-onset neonatal sepsis,” by Kathryn A. Knoop et al.

MEDIA CONTACT: Kathryn A. Knoop, Mayo Clinic, Rochester MN; e-mail:

[email protected]