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Placental Acquisition of Maternal Specific IgG and Helicobacter pylori Colonization in Infancy
Author(s) -
Bunn James E. G.,
Thomas Julian E.,
Harding Marilyn,
Coward W. Andrew,
Weaver Lawrence T.
Publication year - 2003
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1046/j.1523-5378.2003.00178.x
Subject(s) - helicobacter pylori , cord blood , colonization , antibody , placenta , immunoglobulin g , immunology , medicine , immune system , passive immunity , immunoglobulin a , physiology , pregnancy , biology , fetus , microbiology and biotechnology , colostrum , genetics
Background. Colonization with Helicobacter pylori generally occurs in infancy, and the microorganism is often acquired from close family members. Rate of infant colonization may be affected by maternal immune status. Methods. To investigate the potential protective effect of anti‐ H. pylori immunoglobulin G (IgG) acquired via the placenta, 65 mothers and their infants were studied from the infant's birth for 1 year. Circulating IgG antibodies were measured by enzyme‐linked immunosorbent assay (ELISA) in cord blood and every 8 weeks. Immunoblotting was performed on sera from infants with significant increases in IgG levels. Rate of infant H. pylori colonization was measured by 13 C urea breath tests every 4 weeks from the age of 12 weeks. Results. Maternal and infant cord blood specific IgG levels were correlated ( R 2 = .747, p < .001). Infant H. pylori specific IgG fell 5‐fold compared to maternal levels over the first 6 months of life, and rose subsequently in many cases, with the development of novel immunoblot patterns. There were no significant associations between the age at first positive urea breath test and maternal or infant cord specific H. pylori IgG levels. Conclusions. Transplacentally acquired specific IgG antibody does not protect infants from colonization by H. pylori .