Allergic Airway Hyperresponsiveness (AHR)Induced by Aspergillus Fumigatus (Af) Is Attenuated in C57BI.]6 Mice Genetically Deficient of Surfactant Protein (SP)-D

Ref ID: 14397

Author: Angela Haczku*, Elena N Atochina*, Yaniv Tomer*, Seth T Scan/on*, Francis R Poulain§, Samuel Hawgood§, Michael F Beers*

Author address:

*University of
Pennsylvania, Philadelphia, PA §UCSE San Francisco, CA

Full conference title:

2002 American Academy of Allergy, Asthma, and Immunology Annual Meeting

Date: 1 March 2014


SP-D is a member of the pattern-recognition receptor family and may
play an important role in uptake and presentation of allergenic molecules,
such as particles of the fungus Af. The effects of intraperitoneal sensitization
and subsequent intranasal challenges with Af were compared between
SP-D deficient and wild type C57BL/6 mice. Lung function was measured
using whole body plethysmography and the cellular and cytokine content
of airways of the bronchoalveolar lavage (BAL) was analyzed. Production
of surfactant proteins was assessed in the small and large aggregate fractions
of the cell free BAL fluid. Wild-type C57BL/6 mice sensitized
intraperitoneally and challenged intranasally with Af extract showed signifcant
AHR to metacholine (MCh) when compared with naive control
mice (p<0.0001 ANOVA). AHR was associated with markedly increased serum total and Af-specific IgE and IgG 1 levels, a peribronchial/perivascular tissue inflammation, airway eosinophilia and secretion of IL-4 and IL-5 into the BAL fluid. In addition, Af sensitization and challenge induced significant increases in SP-D levels (p<0.01) and decreases in SP-B and SP-C (p<0.05) in the BAL fluid indicating that allergic inflammation is associated with specifically altered surfactant protein expression. Sensitization and challenge of mice deficient in SP-D resulted in a significantly attenuated AHR (p<0.0001 ANOVA) when compared with wild-type mice. The levels of eosinophils, IL-4, IL-5 and eotaxin were also attenuated in the BAL fluid of SP-D deficient mice in comparison with wild-type controls (p<0.05 each). Our data indicate that lack of SP-D significantly impaired the ability of mice to mount allergic airway inflammation upon sensitization and challenge with Af. We speculate that presence of SP-D is required for the development of allergic sensitization and the consequent airway inflammatory responses. Funded by: Francis Families Foundation (AH) and NIH# HL64520 (MFB).

Abstract Number: S168

Conference Year: 2002

Link to conference website: NULL

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