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Helicobacter infection in the surfactant protein D-deficient mouse

Lookup NU author(s): Dr Amy AndersonORCiD


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BACKGROUND: Surfactant protein D (SP-D), a component of innate immunity, is expressed in the gastric mucosa and is up-regulated in the presence of Helicobacter infection. SP-D binds to Helicobacter in vitro, suggesting the involvement of SP-D in Helicobacter-induced immune responses. The aim of this study was to determine the role of SP-D in gastric epithelial defense in vivo. METHODS: Specific pathogen-free SP-D-deficient mice (SP-D(-/-)) and C57BL/6 wild-type controls were challenged by gavage with different doses of Helicobacter felis, a mouse-adapted Helicobacter strain. Mice were assessed for colonization rates and density of infection. Inflammatory responses were measured by neutrophil counting and T-cell responses by proliferation assays on spleen cells stimulated with H. felis sonicate. The in vitro effect of SP-D on Helicobacter uptake by monocyte-derived dendritic cells was assessed by confocal microscopy and FACS analyses. RESULTS: SP-D(-/-) mice were more susceptible to low-dose infectious challenge than C57BL/6 controls (p = .02). The density of colonization was higher in the SP-D(-/-) infected mice. Neutrophil infiltrates were lower in the SP-D(-/-) mice, particularly in the acid-secreting regions of the stomach. T-cell proliferative responses to Helicobacter antigen were reduced in SP-D(-/-) mice (p = .001) after 12 weeks infection. In vitro uptake of Helicobacter by dendritic cells was significantly enhanced in the presence of SP-D (p = .001). CONCLUSION: In the absence of SP-D, Helicobacter uptake by dendritic cells is impaired. This provides an explanation for the diminished inflammation and immune responses in the SP-D(-/-) mice.

Publication metadata

Author(s): Khamri W, Worku ML, Anderson AE, Walker MM, Hawgood S, Reid KBM, Clark HW, Thursz MR

Publication type: Article

Publication status: Published

Journal: Helicobacter

Year: 2007

Volume: 12

Issue: 2

Pages: 112-123

ISSN (print): 1083-4389

ISSN (electronic): 1523-5378

Publisher: John Wiley & Sons, Inc.


DOI: 10.1111/j.1523-5378.2007.00480.x

Notes: Journal Article Research Support, Non-U.S. Gov't United States


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