title: Breast milk fatty acids may link innate and adaptive immune regulation: analysis of soluble CD14, prostaglandin E2, and fatty acids.
abstract: In addition to its role in sensing intraluminal microbial antigens, soluble (s)CD14 may regulate immune responses by its lesser known function as a lipid carrier with possible influences in the production of fatty acid-derived eicosanoids. We investigated the interrelations of fatty acids, prostaglandin E2 (PGE2), and sCD14 and their role in infant atopic eczema during the first year of life. Serum and breast milk samples from mothers and serum samples from their infants were collected at infant's age 3 mo and analyzed for sCD14 and PGE2 concentrations and for fatty acid compositions. The main correlation of sCD14 was with arachidonic acid (20:4n-6) (AA). Dihomo-gamma-linolenic acid (20:3n-6) (DHGLA) and the ratio of n-6 to n-3 fatty acids correlated positively and docosahexaenoic acid (22:6n-3) (DHA) and sum of n-3 fatty acid negatively with PGE2 in mother's serum and linoleic acid (LA) negatively with PGE2 in breast milk. Soluble CD14 tended to be higher and LA, total polyunsaturated fatty acid (PUFA), and sum of n-6 fatty acids were lower in breast milk received by infants with atopic eczema compared with those without. These results suggest that fatty acids contribute to the regulation of innate and adaptive immune responses and link intraluminal exposures, mother's diet, and microbes.
authors.affiliation: Department of Paediatrics, Turku University Central Hospital, 20521 Turku, Finland. kirsi.laitinen@utu.fi
authors.forename: Kirsi
authors.initials: K
authors.lastname: Laitinen
authors.forename: Ulla
authors.initials: U
authors.lastname: Hoppu
authors.forename: Mari
authors.initials: M
authors.lastname: Hämäläinen
authors.forename: Kaisa
authors.initials: K
authors.lastname: Linderborg
authors.forename: Eeva
authors.initials: E
authors.lastname: Moilanen
authors.forename: Erika
authors.initials: E
authors.lastname: Isolauri
mesh_terms: D000328:Adult; D015331:Cohort Studies; D003876:Dermatitis, Atopic / Q000209:etiology* / Q000276:immunology; D015232:Dinoprostone / Q000097:blood / Q000378:metabolism*; D005227:Fatty Acids / Q000097:blood / Q000737:chemistry / Q000378:metabolism*; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology; D007113:Immunity, Innate; D007112:Immunity, Maternally-Acquired; D007223:Infant; D007231:Infant, Newborn; D018950:Lipopolysaccharide Receptors / Q000097:blood / Q000378:metabolism*; D008895:Milk, Human / Q000276:immunology* / Q000378:metabolism*; D011247:Pregnancy; D012995:Solubility
chemical_list: D005227:Fatty Acids; D018950:Lipopolysaccharide Receptors; D015232:Dinoprostone