Human milk IgA promotes normal immune development by limiting Th17-inducing <i>Erysipelatoclostridium ramosum</i> in the infant gut

K Katherine Donald (Department of Microbiology and Immunology, University of British Columbia) A Antonio Serapio-Palacios (Department of Microbiology and Molecular Genetics, University of California) T Tahereh Bozorgmehr (Michael Smith Laboratories, University of British Columbia) M Mandi Ma (Department of Microbiology and Immunology, University of British Columbia) M Ma Andrea Isabelle Garcia (Department of Microbiology and Immunology, University of British Columbia) C Charisse Petersen (Department of Pediatrics, British Columbia Children’s Hospital, University of British Columbia) P Piushkumar Mandhane (Department of Pediatrics, University of Alberta) P Padmaja Subbarao (Translational Medicine Program, The Hospital for Sick Children) T Theo J. Moraes (Translational Medicine Program, The Hospital for Sick Children) E Elinor Simons (Section of Allergy and Immunology, Department of Pediatrics and Child Health, University of Manitoba) S Stuart Turvey (Department of Microbiology and Immunology, University of British Columbia) M Meghan B. Azad (Department of Immunology, University of Manitoba) B B. Brett Finlay (Department of Microbiology and Immunology, University of British Columbia)

Abstract

The gut microbiota is highly dynamic during the first year of life and plays a crucial role in immune development. Breastfeeding is known to support infant health, but the contributions of the numerous breastmilk components to gut microbiota and immune maturation remain unclear. Secretory IgA (SIgA), the most abundant antibody in human milk, is a key modulator of gut microbiota composition. We have shown previously that mouse milk SIgA protects against asthma by limiting segmented filamentous bacteria in mice. The present study uncovers a similar mechanism in humans. Using human milk from the CHILD Cohort Study, we define a relationship between human milk SIgA and infant gut microbiota composition. This leads to the identification of Erysipelatoclostridium ramosum as a key player in immune development, which is controlled by milk SIgA. Cell culture modeling demonstrates that SIgA restricts the capacity of E. ramosum to adhere to the intestinal epithelium and to induce Th17 responses, which are implicated in allergic and other chronic diseases.

Article Details

Volume / Issue Vol. 122, Issue 28
Published July 15, 2025
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (13)

K

Katherine Donald

Department of Microbiology and Immunology, University of British Columbia

A

Antonio Serapio-Palacios

Department of Microbiology and Molecular Genetics, University of California

T

Tahereh Bozorgmehr

Michael Smith Laboratories, University of British Columbia

M

Mandi Ma

Department of Microbiology and Immunology, University of British Columbia

M

Ma Andrea Isabelle Garcia

Department of Microbiology and Immunology, University of British Columbia

C

Charisse Petersen

Department of Pediatrics, British Columbia Children’s Hospital, University of British Columbia

P

Piushkumar Mandhane

Department of Pediatrics, University of Alberta

P

Padmaja Subbarao

Translational Medicine Program, The Hospital for Sick Children

T

Theo J. Moraes

Translational Medicine Program, The Hospital for Sick Children

E

Elinor Simons

Section of Allergy and Immunology, Department of Pediatrics and Child Health, University of Manitoba

S

Stuart Turvey

Department of Microbiology and Immunology, University of British Columbia

M

Meghan B. Azad

Department of Immunology, University of Manitoba

B

B. Brett Finlay

Department of Microbiology and Immunology, University of British Columbia