Breastfeeding Is Associated with Lower Likelihood of Helicobacter Pylori Colonization in Babies, Based on a Prospective USA Maternal-Infant Cohort

Abstract

Background: Mother-to-child transmission of Helicobacter pylori (H. pylori) is the primary source of intrafamilial spread in early childhood in regions of high H. pylori prevalence. However, early-in-life H. pylori colonization and associated protective or risk factors have not been fully evaluated in lower prevalence regions, such as the USA.

Aims: Therefore, from a well-characterized prospective US cohort, we selected women who provided fecal samples during pregnancy and had paired fecal samples from their babies up to 24 months postpartum. We evaluated maternal and baby factors associated with likelihood of H. pylori colonization in the babies. Fecal antigen testing was used to determine H. pylori status. We also evaluated the association between maternal breastmilk cytokines and H. pylori colonization in breastfed babies.

Results: Among included mother-baby pairs (n = 66), H. pylori prevalence was 31.8% in mothers and 19.7% in their babies. Dominant breastfeeding (adjusted odds ratio [aOR] 0.17, 95% CI 0.03-0.98) and maternal IBD (aOR 0.05, 95% CI 0.01-0.27) were associated with significantly lower likelihood of H. pylori colonization among babies; no other clinical factors were associated with H. pylori colonization in the babies. Matrix metalloproteinase-10 (MMP-10) and tumor necrosis factor-related activation-induced cytokine expression were significantly higher in breastmilk of mothers with H. pylori positive vs negative babies.

Conclusions: Consistent with data from high H. pylori prevalence regions, our findings suggest dominant breastfeeding may protect against early H. pylori colonization. Downregulation of pro-inflammatory cytokines such as MMP-10 may be relevant in mediating this protection among breastfed babies, but more data are needed.

Keywords: Antibiotics; Breastfeeding; Cytokines; Helicobacter pylori; Immunomodulation; Infectious diseases.

Figure 1.. Mapping of H. pylori status within mother-baby dyads.

H. pylori status in 66 mothers and their babies at 1 month, 3 months, 12 months, and 24 months along with maternal and baby clinical variables.

Figure 2.. Mapping of H. pylori status within families.

Eleven distinct families had fecal samples and additional information available for other first-degree related household members (fathers, siblings). The results of H. pylori testing by family is depicted. “F” refers to “Family”, while the associated number corresponds to the numeric mother-baby dyad of the 66 total dyads including in the study.

Figure 3.. Maternal breastmilk cytokines differentially expressed in mothers of H. pylori positive vs negative babies, based on PLS-DA supervised clustering model.

PLS-DA supervised clustering model was used to select the most differentially expressed maternal breastmilk cytokines between H. pylori positive vs. negative breastfed babies. Figure 3A. Supervised PLS-DA analysis demonstrated significantly differential clustering by H. pylori status (p-value=0.01). Figure 3B. A total of 14 cytokines were significantly differentially expressed, as determined based on VIP scores>1.5 (see text).