1997
DOI: 10.3109/00365529709025094
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Gastric Juice Levels of Lactoferrin andHelicobacter pyloriInfection

Abstract: This study showed for the first time that Lf is present in gastric juice and that it correlates with H. pylori infection. Lf may constitute a good marker for H. pylori-associated gastritis. Although correlation does not prove causation, this study suggests that Lf might play an important role in the physiopathology of H. pylori-associated gastritis.

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Cited by 33 publications
(19 citation statements)
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“…23 A 70-kDa LF-binding protein highly specific for human LF was identified in outer membrane proteins of H. pylori grown under iron-limiting conditions, and this might constitute the iron uptake system of H. pylori. 24 Because the human LF concentration is estimated to be less than 0.05 mg/ml in gastric juice, 25,26 it is plausible to assume that a high dosage of orally administrated bLF might sequester iron from human LF in the stomach, resulting in inhibition of the growth of H. pylori. Also, recombinant human LF exerted an antibacterial action against 8 of 13 clinical isolates of H. pylori tested in vitro, but 5 of 13 strains were resistant to a high concentration (3 mg/ml) of recombinant human LF.…”
Section: Discussionmentioning
confidence: 99%
“…23 A 70-kDa LF-binding protein highly specific for human LF was identified in outer membrane proteins of H. pylori grown under iron-limiting conditions, and this might constitute the iron uptake system of H. pylori. 24 Because the human LF concentration is estimated to be less than 0.05 mg/ml in gastric juice, 25,26 it is plausible to assume that a high dosage of orally administrated bLF might sequester iron from human LF in the stomach, resulting in inhibition of the growth of H. pylori. Also, recombinant human LF exerted an antibacterial action against 8 of 13 clinical isolates of H. pylori tested in vitro, but 5 of 13 strains were resistant to a high concentration (3 mg/ml) of recombinant human LF.…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, the acquisition of iron plays a critical role in the host interaction with pathogenic bacteria, which have in consequence developed speci®c strategies for iron uptake. In the gastric mucosa, the amount of free ferric iron should be restricted due to the presence of secreted lactoferrin which removes iron by sequestration [26,27]. The presence of speci®c uptake systems for acquisition of iron from host-borne and nutritional sources, including lactoferrin [15,21], transferrin [40], citrate [21,40], and hemin [21,40,45,46] in H. pylori indicates that the iron acquisition of the pathogen is highly adapted to this unusual environment.…”
Section: Introductionmentioning
confidence: 99%
“…Sequestration of iron in lactoferrin in the gastric mucosa is also suggested as possible. 15,16 In our study, 76 of 102 (74.50%) patients with IDA were H. pylori positive. Majority of the cases (53.32%) were in the age group of 20 -39 years.…”
Section: Hb (Gm%)mentioning
confidence: 51%