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dc.contributor.authorMurray, E.
dc.date.accessioned2018-08-24T08:25:50Z
dc.date.available2018-08-24T08:25:50Z
dc.date.issued2002-03-01
dc.identifier.citationMurray, E. (2002). Expression of surfactant protein d in the human gastric mucosa and during helicobacter pylori infection. Infection and Immunity 70 (3), 1481-1487
dc.identifier.issn0019-9567
dc.identifier.urihttp://hdl.handle.net/10379/9613
dc.description.abstractHelicobacter pylori establishes persistent infection of gastric mucosa with diverse clinical outcomes. The innate immune molecule surfactant protein D (SP-D) binds selectively to microorganisms, inducing aggregation and phagocytosis. In this study, we demonstrated the expression of SP-D in gastric mucosa by reverse transcription-PCR and immuohistochemical analysis. SP-D is present at the luminal surface and within the gastric pits, with maximal expression at the surface. Levels of expression are significantly increased in H. pylori-associated gastritis compared to those in the normal mucosa. Immunofluorescence microscopy was used to demonstrate binding and agglutination of H. pylori by SP-D in a lectin-specific manner. These activities resulted in a 50% reduction in the motility of H. pylori, as judged on the basis of curvilinear velocity measured by using a Hobson BacTracker. Lipopolysaccharides extracted from three H. pylori strains were shown to bind SP-D in a concentration-dependent manner, and there was marked variation in the avidity of binding among the strains. SP-D may therefore play a significant role in the innate immune response to H. pylori infection.
dc.publisherAmerican Society for Microbiology
dc.relation.ispartofInfection and Immunity
dc.subjectalveolar macrophages
dc.subjectaspergillus-fumigatus
dc.subjectescherichia-coli
dc.subjectbinding-protein
dc.subjectmotility
dc.subjectlipopolysaccharides
dc.subjectphagocytosis
dc.subjectcolonization
dc.subjectmorphology
dc.subjectallergens
dc.titleExpression of surfactant protein d in the human gastric mucosa and during helicobacter pylori infection
dc.typeArticle
dc.identifier.doi10.1128/iai.70.3.1481-1487.2002
dc.local.publishedsourcehttp://iai.asm.org/content/70/3/1481.full.pdf
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