Scientists Reveal How Breastfeeding Transfers Immunity to Babies

A research team at BYU-Harvard-Stanford has identified a molecule that is key to mothers' ability to pass along immunity to intestinal infections to their babies through breast milk.

A molecule that is key to mothers' ability to pass along immunity to intestinal infections to their babies through breast milk has been identified by a research team at BYU-Harvard-Stanford.

The study has shed light on an amazing change that takes place in a mother's body when she begins producing breast milk.

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For years before her pregnancy, cells that produce antibodies against intestinal infections travel around her circulatory system as if it were a highway and regularly take an "off-ramp" to her intestine.

There they stand ready to defend against infections such as cholera or rotavirus. But once she begins lactating, some of these same antibody-producing cells suddenly begin taking a different "off-ramp," so to speak, that leads to the mammary glands.

That way, when her baby nurses, the antibodies go straight to his intestine and offer protection while he builds up his own immunity.

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Until now, scientists did not know how the mother's body signalled the antibody-producing cells to take the different off-ramp. The new study identifies the molecule that gives them the green light.

Understanding the role of the molecule, called CCR10, also has implications for potential future efforts to help mothers better protect their infants.

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"This tells us that this molecule is extremely important, so if we want to design a vaccine for the mother so she could effectively pass protective antibodies to the child, it would be absolutely essential to induce high levels of CCR10," said Eric Wilson, the Brigham Young University microbiologist who is the lead author on the study.

For the study, the researchers used so-called "knock-out mice" that had been genetically engineered to lack the CCR10 molecule.

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Whereas normal lactating mice had hundreds of thousands of antibody-producing cells in their mammary glands, the BYU team found that the knock-out mice had more than 70 times fewer such cells. Tests verified that the absence of CCR10 was responsible for the deficiency.

The research also showed that CCR10 does not play the same crucial role in signaling antibody-producing cells to migrate to the intestine. Another molecule is their "traffic light."

The findings will be published in the Nov. 1 issue of the Journal of Immunology.

Source-ANI
RAS/SK