Photo Credit: Gorodenkoff

Researchers concluded that vedolizumab (vedo) gut-specific targeting spared passive immunity in lactating mothers with Crohn’s disease (CD) or ulcerative colitis (UC), suggesting alternative homing pathways for antibody-secreting cells to the mammary gland.

The following is a summary of “Vedolizumab Does Not Alter Immunoglobulin Levels in Breastmilk of Mothers with IBD,” published in the January 2024 issue of Gastroenterology by Crohn’s & Colitis Congress 2024.

To safeguard against gut pathogens, breastfeeding leverages maternal antibody-secreting cells (ASCs) educated in the gut and recruited to the lactating mammary gland (LMG) via a specific integrin (a4b7) and its ligands (MAdCAM-1, CCL28). Vedolizumab (vedo) disrupts this recruitment by blocking a crucial site on a4b7.

Researchers performed a retrospective study to determine if vedo, a gut-targeting therapy, disrupts antibody-producing cell homing to the  LMG, potentially impacting breast milk immunoglobulin (Ig) levels.

They assessed Ig levels via ELISA in frozen breast milk from participants in the Mommy’s Milk biorepository at the University of California, San Diego. This included mothers with and without Ulcerative Colitis (UC) or Crohn’s Disease (CD), as well as breastfeeding mothers with UC and CD who underwent vedo treatment for over 18 months. Milk samples were gathered within the time frame of 1 to 15.45 months postpartum.

The results showed that secretory IgA (SIgA) levels in the breast milk of mothers without Inflammatory Bowel Disease (IBD) (n=45) were similar to those of mothers with CD not on vedo (n=15) (301 ± 147 ug/mL vs. 322 ± 207 ug/mL). However, mothers with UC not on vedo (n=7) exhibited lower SIgA levels than non-IBD controls (213 ± 149 ug/mL vs. 301 ± 147 ug/mL, P<0.01). When comparing milk SIgA from patients with CD and UC treated with vedo (CD: n= 9; 256 ± 80 ug/mL, UC: n=10; 283 ± 87 ug/mL) with non-IBD controls (n=45; 301 ± 147 ug/mL), no differences were found. Similarly, SIgA levels were not different between CDs with or without vedo (256 ± 80 ug/mL vs. 322 ± 207 ug/mL). However, SIgA levels in patients with UC with vedo were unexpectedly higher than UC without vedo (283 ±87 ug/mL vs 213 ± 149 ug/mL, P<0.05). No significant differences in secretory IgM levels in milk were found between mothers with UC or CD treated with vedolizumab and non-IBD controls. (65 ± 34 ug/mL, 69 ± 32 ug/mL, and 56 ± 37 ug/mL, respectively). Similarly, no significant difference was observed between patients with UC or CD not treated with video compared with non-IBD controls (58±26 ug/mL and 46 ± 24 ug/mL, respectively).

They concluded that vedo gut-specific targeting spared passive immunity in lactating mothers, suggesting alternative homing pathways for antibody-secreting cells to the mammary gland.