OBJECTIVE: To quantify microbial contamination of human milk purchased via the Internet as an indicator of disease risk to recipient infants. METHODS: Cross-sectional sample of human milk purchased via a popular US milk-sharing Web site (2012). Individuals advertising milk were contacted to arrange purchase, and milk was shipped to a rented mailbox in Ohio. The Internet milk samples (n = 101) were compared with unpasteurized samples of milk donated to a milk bank (n = 20). RESULTS: Most (74%) Internet milk samples were colonized with Gram-negative bacteria or had >104 colony-forming units/mL total aerobic count. They exhibited higher mean total aerobic, total Gram-negative, coliform, and Staphylococcus sp counts than milk bank samples. Growth of most species was positively associated with days in transit (total aerobic count [log10 colony-forming units/mL] β = 0.71 [95% confidence interval: 0.38–1.05]), and negatively associated with number of months since the milk was expressed (β = −0.36 [95% confidence interval: −0.55 to −0.16]), per simple linear regression. No samples were HIV type 1 RNA-positive; 21% of Internet samples were cytomegalovirus DNA-positive. CONCLUSIONS: Human milk purchased via the Internet exhibited high overall bacterial growth and frequent contamination with pathogenic bacteria, reflecting poor collection, storage, or shipping practices. Infants consuming this milk are at risk for negative outcomes, particularly if born preterm or are medically compromised. Increased use of lactation support services may begin to address the milk supply gap for women who want to feed their child human milk but cannot meet his or her needs.

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Food ingestion generally induces antigen (Ag)-specific tolerance rather than immunity. Consistent with this, induction of IgE-mediated intestinal FA in mice has required either Ag priming through a parenteral route or ingestion of Ag with a potent toxin. In contrast, we recently reported (JACI, 131:442-50, 2013) that Ag-specific, IgE-mediated FA is induced when a protein Ag is ingested with the widely used nutrient, MCT. We also showed that MCT ingestion induces increased epithelial cell expression of the pro-Th2 cytokines TSLP, IL-25 and IL-33. We now report that MCT ingestion, by itself, can induce shock by damaging intestinal epithelium, with a consequent increase in intestinal permeability. In contrast, ingestion of the anionic detergent, sodium dodecyl sulfate, damages intestinal epithelium but does not promote a Th2 response. Both direct MCT induction of intestinal epithelial damage and MCT promotion of a Th2 response and FA to co-ingested egg white are suppressed in mice treated with the lipase inhibitor orlistat, which blocks intestinal triglyceride absorption. Consistent with MCT induction of TSLP, IL-25 and IL-33, treatment with a cocktail of mAbs to these cytokines or their receptors blocks FA induction by ingested MCT plus egg white. Taken together, these observations suggest that MCT must be absorbed to damage epithelial cells and induce the pro-Th2 cytokines that promote FA development; they also provide a potential paradigm for natural FA development.