Increased surfactant protein D in rat airway goblet and Clara cells during ovalbumin-induced allergic airway inflammation.
BACKGROUND
Structural remodelling of airways in asthma that follows inflammation may be affected by surfactant protein D (SP-D)-mediated effects on the immune response.


OBJECTIVE
To determine potential sites of SP-D interaction with the pulmonary immune response, we examined the distribution of immunoreactive SP-D in an experimental model of allergen-induced airway inflammation using immunohistochemistry, biochemical methods and in situ hybridization.


METHODS
The experimental model used subcutaneous injection of ovalbumin in adult rats, which induced an airway response to inhaled nebulized ovalbumin. Three groups of rats (ovalbumin, ovalbumin + dexamethasone and saline) were challenged thrice weekly for 3 weeks. A fourth group of seven rats (naive) were taken from the same delivery of rats as the other groups. Lungs were then lavaged to determine total cell count, eosinophil count, ovalbumin-specific IgE by enzyme-linked immunosorbent assay and SP-D by immunoblot. Tissue samples were fixed and embedded, and sections were studied for the infiltration of eosinophils and for expression of SP-D protein by histochemistry and mRNA by in situ hybridization.


RESULTS
Ovalbumin induced perivascular and peribronchiolar eosinophilia which could be prevented by dexamethasone treatment. In addition, the ovalbumin-specific IgE levels in serum and bronchoalveolar lavage fluid of ovalbumin-challenged animals were enhanced. Increased amount of SP-D in lavage and tissue, particularly in type II pneumocytes, in Clara cells and, surprisingly, in hyperplastic goblet cells of inflamed lungs was found. SP-D mRNA was detected in goblet cells as well as in type II pneumocytes and Clara cells. Dexamethasone treatment did not affect level of SP-D immunoreactivity.


CONCLUSIONS
SP-D accumulation is increased in this model of allergen-induced eosinophilia, both in upper and lower airways. The increase is unaffected by dexamethasone.
Kasper
M
M
Institutes of Anatomy, Medical Faculty 'Carl Gustav Carus', Technical Universtiy of Desden, Dresden, Germany.
Sims
G
G
Koslowski
R
R
Kuss
H
H
Thuemmler
M
M
Fehrenbach
H
H
Auten
R L
RL
D000704:Analysis of Variance; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001249:Asthma / Q000276:immunology / Q000378:metabolism*; D015153:Blotting, Western / Q000379:methods; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D003907:Dexamethasone / Q000627:therapeutic use; D004804:Eosinophils / Q000276:immunology; D020397:Goblet Cells / Q000737:chemistry*; D007073:Immunoglobulin E / Q000032:analysis / Q000097:blood; D007150:Immunohistochemistry / Q000379:methods; D017403:In Situ Hybridization; D007958:Leukocyte Count; D008297:Male; D023421:Models, Animal; D010047:Ovalbumin; D037663:Pulmonary Surfactant-Associated Protein D / Q000032:analysis*; D051381:Rats; D011914:Rats, Inbred BN
D000893:Anti-Inflammatory Agents; D037663:Pulmonary Surfactant-Associated Protein D; D007073:Immunoglobulin E; D003907:Dexamethasone; D010047:Ovalbumin