Maternal antibodies protect against newborn infection

Maternal antibodies may protect babies from severe newborn infection caused by E. coli, after a study found the sickest infants had far lower levels.

A multi-centre study has shed new light on why some newborns become severely ill from Escherichia coli, or E. coli, while others do not.

The findings suggest most babies are protected by germ-fighting antibodies passed on by their mothers.

Sing Sing Way, an expert on immune system changes in expecting mothers and babies in the division of infectious diseases at Cincinnati Children’s and senior author on the study, said: “This helps explain a long-standing question: if most babies are exposed to germs soon after birth, why don’t even more develop severe infection?

“Our findings provide a key missing piece to this puzzle, the antibodies stimulated by the presence of these common bacteria in our intestines protect us against infection. 

“In pregnancy, the natural transfer of these germfighting antibodies from mothers to babies in the womb protect the vast majority against infection.

“In the rare situation when these antibodies are low in mothers or inefficiently transferred, babies are at much higher risk for infection.”

The study examined why only some babies develop severe infection from common bacteria.

E. coli is a common bacterium that lives in the intestines of nearly all people and is a leading cause of severe infection in newborn babies.

The research found that the babies who became most severely ill from E. coli infection also had markedly lower levels of germ-fighting antibodies transferred from their mothers.

The multi-centre research was led by Cincinnati Children’s, in collaboration with the University of Queensland in Australia, the University of Texas Southwestern Medical Center, Children’s Mercy Kansas City and the University of Missouri Kansas City School of Medicine.

To conduct the study, researchers retrieved dried blood samples collected during routine newborn screening from 100 babies who eventually developed E. coli infection and compared their antibody levels with those of hundreds of other infants who did not.

The analysis found that antibodies targeting E. coli were consistently reduced in infected babies. Because E. coli can vary widely, the researchers used a panel of strains isolated from infected babies to assess levels of these germ-fighting antibodies.

In a separate part of the study, the researchers used mice raised without any exposure to E. coli and therefore lacking the relevant antibodies.

They found that introducing a probiotic strain of E. coli, called Nissle 1917, to mice before pregnancy stimulated production of protective antibodies that efficiently protected newborn mice against infection.

The probiotic is widely available for human use in Europe, Asia and Australia under the trade name Mutaflor.

Mark Schembri, co-author and researcher at the Institute for Molecular Bioscience at the University of Queensland, said: “Understanding protection takes both types of evidence, what we can evaluate from specimens in human babies that naturally develop infection, and what we can test by experimentally causing infection.

“By strategically combining real-world human newborn screening samples with carefully designed infection models, we can start to pinpoint which antibody targets matter most and how broad protection might be achieved.”

Susana Chavez-Bueno, co-author from Children’s Mercy Hospital in Kansas City, said: “Neonatal sepsis can escalate quickly, and clinicians need better ways to identify which infants are at highest risk. These findings suggest a path toward earlier risk recognition and eventually, prevention strategies built around restoring the missing protective maternal antibodies.”

The researchers said they plan to develop a screening test to identify newborns at highest risk of severe E. coli infection, and eventually a probiotic that could be safe for mothers and strengthen their own immunity as well as the immunity transferred to their babies.