Abstract • 3

While it is clear that a primary effect of human milk feeding is protection of the infant against infectious morbidity and mortality, the mechanisms important for achieving this effect remain less clear. Although human milk contains well-recognized host defense components such as leukocytes, immunoglobulins, complement and pro-inflammatory cytokines, careful examination of the character, content and function of these components reveals they are unlikely to be active participants in classic host defense mechanisms. Milk also contains components (many of them glycosylated) that likely contribute to milk-mediated protection against infection via predominantly preventative mechanisms. The third, less well appreciated component of milk-mediated protection against symptomatic infection is its anti-inflammatory character. Milk exerts direct anti-inflammatory effects through suppression of inflammatory cell function, suppression of pro-inflammatory cytokine function and promotion of healing/growth. Suppression of inflammatory cell function appears to occur via inappropriate cellular activation and/or alteration of intracellular Ca++ balance. Suppression of inflammatory cytokine function occurs via endogenous control systems involving soluble receptors and at least one cytokine antagonist. Promotion of healing/growth is achieved through growth factors present in milk. While these effects are most likely to occur at the level of the bowel lumen, it is provocative to consider that absorption of milk components responsible for suppression of inflammatory cell function, blockade of inflammatory cytokine effects and promotion of healing/growth might produce a systemic anti-inflammatory state in the breast-fed infant, resulting in less symptomatic infection scarring responses to injury. The author is located at the Center for Pediatric Research, Children's Hospital of The Kings Daughters and Eastern Virginia Medical School, Norfolk, Virginia, and is supported through NICHHD 13021-19.