Linked Life Data

15905537

Source:http://linkedlifedata.com/resource/pubmed/id/15905537

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2005-5-20
pubmed:abstractText
Lung surfactant protein A (SP-A) and D (SP-D) are innate immune molecules which are known to interact with allergens and immune cells and modulate cytokine and chemokine profiles during host hypersensitivity response. We have previously shown therapeutic effects of SP-A and SP-D using a murine model of lung hypersensitivity to Aspergillus fumigatus (Afu) allergens. In this study, we have examined the susceptibility of SP-A (AKO) or SP-D gene-deficient (DKO) mice to the Afu allergen challenge, as compared with the wild-type mice. Both AKO and DKO mice exhibited intrinsic hypereosinophilia and several-fold increase in levels of IL-5 and IL-13, and lowering of IFN-gamma to IL-4 ratio in the lungs, suggesting a Th2 bias of immune response. This Th2 bias was reversible by treating AKO or DKO mice with SP-A or SP-D, respectively. The AKO and DKO mice showed distinct immune responses to Afu sensitization. DKO mice were found more susceptible than wild-type mice to pulmonary hypersensitivity induced by Afu allergens. AKO mice were found to be nearly resistant to Afu sensitization. Intranasal treatment with SP-D or rhSP-D (a recombinant fragment of human SP-D containing trimeric C-type lectin domains) was effective in rescuing the Afu-sensitized DKO mice, while SP-A-treated Afu-sensitized AKO mice showed several-fold elevated levels of IL-13 and IL-5, resulting in increased pulmonary eosinophilia and damaged lung tissue. These data reaffirm an important role for SP-A and SP-D in offering resistance to pulmonary allergenic challenge.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
174
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6943-54
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15905537-Allergens, pubmed-meshheading:15905537-Animals, pubmed-meshheading:15905537-Antigens, Fungal, pubmed-meshheading:15905537-Aspergillosis, Allergic Bronchopulmonary, pubmed-meshheading:15905537-Aspergillus fumigatus, pubmed-meshheading:15905537-Cells, Cultured, pubmed-meshheading:15905537-Erythropoietin, pubmed-meshheading:15905537-Female, pubmed-meshheading:15905537-Genetic Predisposition to Disease, pubmed-meshheading:15905537-Humans, pubmed-meshheading:15905537-Interleukin-13, pubmed-meshheading:15905537-Interleukin-15, pubmed-meshheading:15905537-Interleukin-5, pubmed-meshheading:15905537-Male, pubmed-meshheading:15905537-Mice, pubmed-meshheading:15905537-Mice, Inbred C57BL, pubmed-meshheading:15905537-Mice, Knockout, pubmed-meshheading:15905537-Pulmonary Eosinophilia, pubmed-meshheading:15905537-Pulmonary Surfactant-Associated Protein A, pubmed-meshheading:15905537-Pulmonary Surfactant-Associated Protein D, pubmed-meshheading:15905537-Recombinant Proteins, pubmed-meshheading:15905537-Serum Albumin, Bovine
pubmed:year
2005
pubmed:articleTitle
Susceptibility of mice genetically deficient in the surfactant protein (SP)-A or SP-D gene to pulmonary hypersensitivity induced by antigens and allergens of Aspergillus fumigatus.
pubmed:affiliation
Institute of Genomics and Integrative Biology, Council for Scientific and Industrial Research, Delhi, India.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't