No abstract

Secretory immunoglobulin A (SIgA) anti-casein and SIgA anti-β-lactoglobulin (BLG) were determined in the saliva of 158 healthy mature infants at birth and in breast milk samples using a direct Elisa technique. IgG anti-casein and anti-BLG were measured in serum samples from mothers and newborns (cord blood). A high risk of allergy was defined in 66 infants who had cord blood (CB)-IgE levels ≥0.9 IU/ml and/or parents with atopic diseases. Thirty infants had CB levels <0.9 IU/ml and parents without clinical symptoms of atopy but with elevated serum IgE concentrations or type I skin reactions to common allergens (low risk). Sixty-two infants had CB-IgE levels <0.9 IU/ml and healthy parents (no risk). The groups were matched for social status, smoking and dietary habits. SIgA anti-casein and anti-BLG were detected in all newborns. SIgA anti-casein was significantly higher (p <0.05) in high risk infants (median 157; 50% confidence limits 45–270) than in no risk (48; 25–150) or low risk infants (43; 21–130). SIgA anti-casein values correlated with maternal allergy, maternal allergy plus CB-IgE, but not with paternal allergy. Breast milk SIgA anti-BLG was depressed (p <0.05) in mothers with manifest allergy compared to healthy mothers. Determination of salivary SIgA anti-casein may represent an additional screening method for early detection of infants with atopic disposition.

One hundred and fifty-eight healthy mature newborns were divided into 3 groups according to their risk of allergy: Group A, no risk (n = 62), group B, low risk (n = 30) and Group C, high risk (n = 66). Saliva was collected at birth and after 3 and 6 months. SIgA anti-casein and anti-beta-lactoglobulin were determined by a direct ELISA technique. The highest concentrations of secretory antibodies were measured after birth. After 3 months, breast fed infants had lower salivary SIgA anti-casein concentrations than the group receiving cow's milk (p less than 0.01). The effect of breast-feeding was seen even after a nursing period of only 3 weeks. Infants without risk of allergy fed cow's milk exclusively had higher SIgA anti-casein (p less than 0.03) and anti-beta-lactoglobulin concentrations than low risk infants at the age of 6 months. These data show a modifying effect of breast feeding on salivary SIgA production against cow's milk protein.

Salivary SIgA antibodies against RS virus were studied in 105 children during the first year of life. The infants were divided into groups according to their risk of atopy. At birth 13 neonates showed measurable amounts of SIgA to RS virus. In another 26 children specific antibodies were detected but in concentrations too low for quantitative analysis. During the first year of life this increased to 29 antibody-positive samples with measurable amounts of antibody and 39 with concentrations too low for quantitative determination. At this time 8 children of the high risk group had developed symptoms of allergy. None of these children had measurable amounts of SIgA anti-RSV in their saliva. In comparison, 10 of the remaining 26 high risk infants without symptoms of allergy did have such antibodies. Atopic infants had significantly more respiratory infections during the first year of life than nonatopic infants. The avidity of SIgA anti-RSV in neonatal samples was significantly higher than avidity determined in breast milk SIgA but comparable to the avidity of serum IgG. During the first year of life a continuing decrease of salivary SIgA avidity was observed.

The sympathetic nervous system is one of the major pathways involved in immune-neuroendocrine interactions. Disturbances in these interactions are likely to have consequences during lymphoproliferative diseases. Work derived from our group as well as from several others led us to the hypothesis that the overstimulation of the immune system that characterizes this type of pathology results in decreased sympathetic nerve activity in lymphoid organs. To explore this possibility, we used as a model lpr/lpr mice, which develop a genetically determined autoimmune, lupus-like lymphoproliferative disease. We show that 18-week-old female C57Bl/6J lpr/lpr mice, which do not show overt symptoms of the disease but already have increased IgM and IgG2a levels in the blood, have decreased noradrenaline (NA) concentration and content in the spleen, but not in the kidney, as compared to normal C57Bl/6J littermates. Lpr/lpr mice do not express normal Fas, and therefore apoptosis cannot be triggered through this receptor. The defects in sympathetic innervation in the spleen of lpr/lpr mice prompted us to evaluate whether NA could influence lymphoid cell mass by inducing apoptosis. We found that NA can directly induce apoptosis in normal lymphoid cells via beta-adrenergic receptors. From the reported results we propose that reduction in sympathetic nerve function in lpr/lpr mice contributes to aggravation of the disease and suggest that in addition to the incapacity to mount Fas-mediated apoptosis, a second proapoptotic mechanism, namely, that triggered by NA, is defective in these animals because of reduced availability of the neurotransmitter.