CYTOKINES, CHEMOKINES, AND COLONY-STIMULATING FACTORS IN HUMAN-MILK -THE 1997 UPDATE

Citation
Rp. Garofalo et As. Goldman, CYTOKINES, CHEMOKINES, AND COLONY-STIMULATING FACTORS IN HUMAN-MILK -THE 1997 UPDATE, Biology of the neonate, 74(2), 1998, pp. 134-142
Citations number
58
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00063126
Volume
74
Issue
2
Year of publication
1998
Pages
134 - 142
Database
ISI
SICI code
0006-3126(1998)74:2<134:CCACFI>2.0.ZU;2-J
Abstract
Epidemiologic studies conducted over the past 30 years to investigate the protective functions of human milk strongly support the notion tha t breast-feeding prevents infantile infections, particularly those aff ecting the gastrointestinal and respiratory tracts. However, more rece nt clinical and experimental observations also suggest that human milk not only provides passive protection, but also can directly modulate the immunological development of the recipient infant. The study of th is remarkable defense system in human milk has been difficult due to i ts biochemical complexity, the small concentration of certain bioactiv e components, the compartmentalization of some of these agents, the dy namic quantitative and qualitative changes of milk during lactation, a nd the lack of specific reagents to quantify these agents. Nevertheles s, a host of bioactive substances including hormones, growth factors, and immunological factors such as cytokines have been identified in hu man milk. Cytokines are pluripotent polypeptides that act in autocrine /paracrine fashions by binding to specific cellular receptors. They op erate in networks and orchestrate the development and functions of the immune system. Several different cytokines and chemokines have been d iscovered in human milk over the past years, and the list is growing v ery rapidly. This article will review the current knowledge about the increasingly complex network of chemoattractants, activators, and anti -inflammatory cytokines present in human milk and their potential role in compensating for the developmental delay of the neonate immune sys tem.