Breast-fed infants have higher bilirubin levels than formula-fed infants, possibly because of variations in the composition of the breast milk. The aim of this study was to investigate whether there is a relationship between cytokine levels in the colostrum of nursing mothers and neonatal jaundice (NJ). Breast milk samples were collected from breast-feeding mothers of healthy fullterm neonates, 32 with NJ and 29 without jaundice. The concentrations of IL-1, IL-6, IL-8, IL-10, and tumor necrosis factor (TNF)-␣ were measured by chemiluminescence enzyme immunometric assays. Mothers of infants with NJ had a higher concentration of IL-1 in colostrum, compared with those feeding neonates without NJ, and similar trends were seen for IL-6, IL-8, IL-10, and for TNF-␣. The concentrations of IL-1 significantly correlated with IL-6, IL-8, IL-10, and TNF-␣ concentrations, but not with serum bilirubin levels of infants with NJ. In conclusion, the concentrations of IL-1 were increased in colostrum from breast-feeding mothers whose infants had NJ. The correlation between the concentrations of cytokines involved in the function of hepatic uptake and excretory systems and in the enterohepatic circulation of bilirubin provides additional data to the delineation of the cascade of pathophysiological events that can lead to NJ. B reast-fed infants have higher bilirubin levels than formula-fed infants (1). The jaundice of breast-fed infants is commonly of undetermined etiology (2-4). Suggested mechanisms for these findings include insufficient milk transfer to the neonate (5), inhibition of hepatic excretion of bilirubin (6), and increased intestinal absorption of bilirubin (7,8).Inhibition of hepatic excretion of bilirubin could explain the jaundice associated with human milk consumption, and early studies suggested that exposure to acquired cholestatic injury such as drugs, hormones, proinflammatory cytokines, or biliary obstruction or destruction results in an altered expression and function of hepatic uptake and excretory systems, changes that may maintain and contribute to cholestasis and jaundice (9). In particular, increased production of IL-8 and IL-10 has been reported in patients with biliary obstruction and jaundice (10,11). Moreover, the cholestatic effect of cytokines (e.g. IL-1, IL-6) is believed to result from the repression of genes that normally mediated the hepatic uptake, metabolism, and biliary excretion of bile salts and various nonbile salt organic anions such as bilirubin (12,13). In addition, IL-1␣, IL-6, and tumor necrosis factor (TNF)-␣ were found to decrease the glucuronidation activities dose dependently (14).Intestinal absorption is a key step in the enterohepatic circulation of bilirubin because bilirubin is more easily absorbed from the intestine than are bilirubin glucuronides. Increased intestinal absorption of bilirubin (15), facilitated by breast milk rich in -glucuronidase (16) or via some other mechanisms such as delayed passage of meconium, the establishment of a population of inte...