Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Decrease of the surface fraction of surfactant proteins containing clara cells and type II pneumocytes in a rat asthma model.

Authors: Schmiedl, A  Tschernig, T  Brasch, F  Pabst, R  Bargsten, G 
Citation: Schmiedl A, etal., Exp Toxicol Pathol. 2005 Mar;56(4-5):265-72.
Pubmed: (View Article at PubMed) PMID:15816355
DOI: Full-text: DOI:10.1016/j.etp.2004.10.004

In asthma surfactant proteins (SP) might differ in distribution and composition and thus play a role in pathophysiology of this disease. Therefore, the well-established animal model of ovalbumin sensitized and challenged rats were used to study the distribution of surfactant proteins in Clara cells and type II pneumocytes. Serial sections of paraffin embedded lung tissue were sequentially immunostained by the avidin-biotin-peroxidase complex (ABC) technique. Antisera against SP-A, SP-B and Clara cell specific protein (CC10) were used. We determined stereologically' the surface fraction of immunolabelled cells and semiquantitatively the percentage of test fields containing labelled alveolar macrophages. In allergen sensitized and provocated rat lungs: (1) the surface fraction of SP-A and SP-B positive Clara cells was significantly reduced, (2) the surface fraction of Clara cells stained with CC10 was coincided with controls, (3) the surface fraction of SP-A and not of SP-B possitive type II pneumocytes decreased significantly, (4) a significantly higher percentage of test fields with SP-A labelled alveolar macrophages was evaluated. Thus, in this animal model of asthma the inflammatory process after allergen challenge is accompanied by alterations in the distribution patterns of SP in Clara cells and type II pneumocytes.

Annotation

Disease Annotations
Objects Annotated

Additional Information

 
CRRD Object Information
CRRD ID: 4143398
Created: 2010-09-22
Species: All species
Last Modified: 2010-09-22
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.