Abstract

124 H. pylori, one of the commonest human bacterial infections, is usually acquired in childhood. We sought evidence for a role of specific matemal milk IgA against H. pylori colonisation in 65 breast fed Gambian infants, in whom H. pylori was diagnosed using monthly13 C UBTs across the first year of life. IgA against crude whole cellH. pylori antigen and recombinant H. pylori urease were measured by immunoassay. 85% of infants developed one or more positive UBTs during their first year of life. For infants born in the first 6 months (n=32), following problems with the village water supply, the median age of colonisation (first positive UBT) was 8 weeks. Following this period it rose to 28 weeks. Mean levels (o.d. ratio) of milk IgA directed against rUrease were lower (p<0.001) in the milk from mothers of infants born in the first 4 months of the study (0.091, 95% Cl 0.71-0.111) than in mothers of infants born thereafter (0.177, 95% Cl 0.163-0.191). Mothers of infants who remained free from colonisation throughout the first year produced significantly higher median levels of anti-rUrease IgA than the other mothers (0.183 vs. 0.135, p=0.027). There was no association found between total IgA or IgA against crude whole cell anti-H. pylori antigen and infants UBT results. The most striking differences in antibody levels occurred during the first 3 months of life, when the milk of mothers of non-colonised children had significantly higher levels of anti-rUrease IgA at 4, 8, and 12 weeks than that of mothers of children who developed early H. pylori colonisation (p<0.005, p<0.005, p<0.25 respectively). The associations, and the temporal relationships between them, provide the first good evidence to support the hypothesis that human breastmilk antibodies directed against H. pylori urease can protect against colonisation in infancy.

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