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Comparison of concentration and avidity of specific antibodies to E. coli in breast milk and serum.

  • F H Sennhauser
  • R A Macdonald
  • D M Roberton
  • C S Hosking
Publication Date
Mar 01, 1989
  • Biology


To investigate the relationship between mucosal and systemic immunity we analysed the specific anti-Escherichia coli antibody concentration and avidity of IgA in colostrum and IgG in paired blood samples from 47 mothers giving birth to premature neonates. The avidity of each sample, expressed as an avidity index, was determined using a novel enzyme immunoassay (EIA)-based procedure, while specific antibody determinations were performed by means of conventional sandwich EIA techniques. All subjects had detectable antibody to E. coli in serum and breast milk. The median avidity index for specific IgA antibody in breast milk (3.53 M NH4SCN, range 2.77-4.90) was significantly higher (P less than 0.0001) than that for specific IgG antibody in serum (median 2.03 M NH4SCN, range 1.15-3.65). Using Spearman correlation analysis, a weak but significant association was found between the avidity of colostral IgA antibody and the avidity of systemic IgG antibody to pooled E. coli polysaccharides (rs = 0.29, P = 0.02). There was also a weak correlation between the concentrations of specific serum IgG antibody and of specific colostral IgA antibody (rs = 0.36, P = 0.006). There was no correlation between the concentration of IgA anti-E. coli antibody in colostrum and the avidity of colostral IgA antibody (rs = 0.14, P less than 0.05). Similarly, there was no correlation between the concentration and the avidity of serum IgG anti-E. coli antibody (rs = 0.23, P less than 0.05). The findings of this study suggest independent regulation of concentration and avidity of specific IgA antibody in preterm breast milk. Similar results were seen for specific IgG antibody in serum. The correlations between systemic and mucosal antibody with respect to both concentration and avidity were significant, but are relatively weak and therefore suggest that there also may be independent factors which afford differential regulation of systemic and mucosal antibody responses.

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