Inhibition of Helicobacter pylori infection by bovine milk glycoconjugates in a BALB/cA mouse model

Department of Infectious Diseases and Medical Microbiology, University of Lund, Lund and *Department of Pathology, Sahlgrenska University Hospital, Gothenburg, Sweden Corresponding author: Professor T. Wadström (e-mail: torkel.wadstrom{at}mmb.lu.se ). Received 31 May 2000; revised version accepted 2...

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Veröffentlicht in:Journal of medical microbiology 2001-05, Vol.50 (5), p.430-435
Hauptverfasser: WANG, X, HIRMO, S, WILLEN, R, WADSTROM, T
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Sprache:eng
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Zusammenfassung:Department of Infectious Diseases and Medical Microbiology, University of Lund, Lund and *Department of Pathology, Sahlgrenska University Hospital, Gothenburg, Sweden Corresponding author: Professor T. Wadström (e-mail: torkel.wadstrom{at}mmb.lu.se ). Received 31 May 2000; revised version accepted 23 Oct. 2000. Abstract The attachment of Helicobacter pylori to the human gastric mucosa is a complex process involving several specific structures recognised by the cell surface receptors. Sialylated multivalent high mol. wt glycoproteins have been shown to inhibit H. pylori sialic acid-specific haemagglutination. This study explored whether sialylated glycoconjugates from bovine milk could inhibit an experimental H. pylori infection in a mouse model. BALB/cA mice (6–8 weeks old) were inoculated with a mouse-passaged H. pylori strain 317p. Four weeks after infection the mice were given lactoferrin (iron-free LF or 20% iron-saturated LF) or bovine milk fat globule membrane fractions (MFGM or defatted MFGM) orally (400 mg/kg body weight) once daily for 10 days and then killed to examine for bacterial colonisation and gastritis. Mice treated with iron-free LF, 20% iron-saturated LF, MFGM or defatted MFGM showed 30%, 10%, 20% or 20% healing rates, respectively, when compared with the H. pylori -infected control. Gastric colonisation by H. pylori was remarkably decreased in all mice treated with bovine milk glycoconjugates and the inflammation score was also significantly lower in treated mice than in infected control animals. The fact that there was no significant difference between iron-free LF and iron-saturated LF or MFGM and defatted MFGM suggested that iron is not crucial for inhibition of H. pylori by lactoferrin and that the lipid part of MFGM is not important for anti- H. pylori activity. In conclusion, bovine milk glycoconjugates showed potencies to inhibit H. pylori infection in this mouse model and, therefore, could be considered as candidates for non-antibiotic strategies against H. pylori infection in man.
ISSN:0022-2615
1473-5644
DOI:10.1099/0022-1317-50-5-430