SOLUBLE ADHESION MOLECULES AND ORAL ANTIGEN FEEDING IN INFANTS

Citation
J. Paronen et al., SOLUBLE ADHESION MOLECULES AND ORAL ANTIGEN FEEDING IN INFANTS, Pediatric research, 40(2), 1996, pp. 276-279
Citations number
22
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00313998
Volume
40
Issue
2
Year of publication
1996
Pages
276 - 279
Database
ISI
SICI code
0031-3998(1996)40:2<276:SAMAOA>2.0.ZU;2-3
Abstract
Oral administration of foreign proteins, e.g. cow's milk (CM) proteins , stimulates the immune system and induces humoral and cellular immune response against these antigens in infants. Up-regulation of adhesion molecules is known to be associated with activation of the immune sys tem. The purpose of the study was to examine whether orally administer ed CM proteins induce elevation in soluble adhesion molecules, i.e. in tercellular adhesion molecule-1 (ICAM-1) and L-selectin, in infants. I n a double-blind trial, 10 infants received CM-based formula and 10 in fants casein hydrolysate formula until the age of 9 mo. The infants of mothers with insulin-dependent diabetes mellitus (IDDM) were recruite d into a pilot study of a trial for primary prevention of IDDM by elim ination of CM proteins from the diet during early infancy. A cord bloo d sample and peripheral blood samples were taken at the ages of 3, 6, 9, and 12 mo of age, The levels of soluble ICAM-1 and L-selectin were measured by ELISA. The levels of soluble ICAM-1 were higher at the age s of 3, 6, 9, and 12 mo in infants who received CM-based formula than in infants who received hydrolyzed formula (p = 0.05). Instead, no dif ference was found in the the levels of soluble L-selectin. The levels of soluble ICAM-1 and L-selectin were higher in all infants when compa red with the levels reported in adults or to the levels seen in cord b lood. Orally fed CM proteins induce an elevation in soluble ICAM-1 in infants. This may reflect the generation of an immune response against these proteins, because ICAM-1 has an important costimulatory role in lymphocyte activation.