BACKGROUND: Once Helicobacter pylori infection is established, it is difficult to eradicate despite a persistent systemic and local immune response. It is not known whether immunisation can be used to prevent H pylori infection in humans. AIMS: To evaluate the effect of the human immune response on adherence of H pylori to gastric cells. METHODS: Human milk from a woman infected with H pylori and milk from a non-infected woman were each fractionated by chromatography on DEAE cellulose. Bacteria were incubated with either serum, human milk, human milk fractions, or secretory IgA before incubation with Kato III cells (cells from a gastric adenocarcinoma cell line). Bacterial adherence to the cells was assessed using flow cytometry. RESULTS: Serum from both the H pylori infected and non-infected women killed H pylori. This resulted from the action of complement as heating the serum to 56 degrees C for 30 minutes abolished the bactericidal activity. Immunoglobulin fractions from serum of both infected and non-infected women did not inhibit H pylori adherence to Kato III cells. Human milk from the woman infected with H pylori and from the non-infected woman inhibited binding of H pylori to Kato III cells by 50 to 70%. Secretory IgA isolated from human milk had minimal inhibitory effect on adherence and this was notably less than the inhibitory effect of whole human milk. CONCLUSIONS: Human milk inhibits adherence of H pylori to Kato III cells and this inhibition is independent of whether or not the donor is infected with H pylori. Secretory IgA has minimal inhibitory effect on H pylori adherence.
BACKGROUND: Once Helicobacter pyloriinfection is established, it is difficult to eradicate despite a persistent systemic and local immune response. It is not known whether immunisation can be used to prevent H pylori infection in humans. AIMS: To evaluate the effect of the human immune response on adherence of H pylori to gastric cells. METHODS:Human milk from a woman infected with H pylori and milk from a non-infected woman were each fractionated by chromatography on DEAE cellulose. Bacteria were incubated with either serum, human milk, human milk fractions, or secretory IgA before incubation with Kato III cells (cells from a gastric adenocarcinoma cell line). Bacterial adherence to the cells was assessed using flow cytometry. RESULTS: Serum from both the H pylori infected and non-infected women killed H pylori. This resulted from the action of complement as heating the serum to 56 degrees C for 30 minutes abolished the bactericidal activity. Immunoglobulin fractions from serum of both infected and non-infected women did not inhibit H pylori adherence to Kato III cells. Human milk from the woman infected with H pylori and from the non-infected woman inhibited binding of H pylori to Kato III cells by 50 to 70%. Secretory IgA isolated from human milk had minimal inhibitory effect on adherence and this was notably less than the inhibitory effect of whole human milk. CONCLUSIONS:Human milk inhibits adherence of H pylori to Kato III cells and this inhibition is independent of whether or not the donor is infected with H pylori. Secretory IgA has minimal inhibitory effect on H pylori adherence.
Authors: B J Rathbone; J I Wyatt; B W Worsley; S E Shires; L K Trejdosiewicz; R V Heatley; M S Losowsky Journal: Gut Date: 1986-06 Impact factor: 23.059
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