Milk proteins, cytokines and intestinal epithelial functions in children.

This paper discusses the relationship between food antigens, lymphocytes and the epithelial properties of the jejunum in children with cow's milk allergy. Experimental results indicate that increased protein permeability is not the primary cause of cow's milk allergy. Rather, results are interpreted as a secondary effect of an abnormal immunological response leading to mucosal inflammation and impairment of the endocytic process by the intestinal epithelial cells. Stimulation by cow's milk proteins caused the lymphocytes from infants with cow's milk allergy to release more tumor necrosis factor-alpha TNF alpha than those from control infants. After appropriate antigenic stimulation, the cytokines released by the activated lymphocytes from these infants perturbed epithelial function, in particular its barrier capacity. Tumor necrosis factor alpha, together with gamma interferon are involved in these adverse effects. It is thought that bovine beta-lactoglobulin present in the intestinal lumen may be responsible for the secretory diarrhea observed in children with cow's milk allergy, as a consequence of stimulation of electrogenic chloride secretion. In addition, luminal foreign protein may stimulate the submucosal cells. As a consequence, the submucosal release of mediators, including lymphokines, might alter the intestinal epithelial barrier. In conclusion, in physiological conditions, the subepithelial tissue that comprises the immune system and many other systemic systems receive information on the antigenic content within the intestinal lumen via the intestinal epithelium.