Abstract: Recombinant surfactant protein A and medicament compositions based thereon are useful for the prevention or treatment of pulmonary infection and inflammation.

Abstract: The present invention provides methods to protect a subject from a respiratory disorder involving an airway obstructive disease such as asthma or chronic obstructive pulmonary disease. Provided are methods to protect a subject from an airway obstructive disease using gene therapy. Methods are provided for supplying FoxA2 function to cells of the lung and airway, such as smooth muscle and epithelial cells, by FoxA2 gene therapy. The FoxA2 gene, a modified FoxA2 gene, or a part of the gene may be introduced into the cell in a vector such that the gene remains extrachromosomal or may be integrated into the subjects chromosomal DNA for expression. These methods provide for administering to a subject in need of such treatment a therapeutically effective amount of a FoxA2 gene, or pharmaceutically acceptable composition thereof, for overexpressing the FoxA2 gene.

Abstract: The discovery that CFTR modifier genes, in particular the Kir4.2 gene, the expressed polypeptide(s), as well as genetic and polypeptide regulators thereof, can be used to treat cystic fibrosis (CF), or at least the conditions that cause CF. Methods and products for detecting and/or identifying CFTR modifier genes, their respective expressed polypeptides, the genetic regulators of such CFTR modifier genes, and the regulators of their respective expressed polypeptides are disclosed. Also disclosed are compositions and methods using these CFTR modifier genes, their respective expressed polypeptides, genetic regulators of these CFTR modifier genes, and/or CFTR modifier polypeptide regulators for the purpose of treating CF, or at least the conditions that cause CF, are disclosed.

Abstract: This invention relates to the discovery that midkine modulates pulmonary vasculature development and smooth muscle cell development. Modulation of midkine activity thus alters pulmonary vasculature development and smooth muscle cell development. The invention provides methods of modulating pulmonary disorders, smooth muscle cell related disorders, and pulmonary smooth muscle cell disorders. Disorders of particular interest include, but are not limited to, asthma and pulmonary hyperplasia. Further the invention relates to the discovery that TTF1 and HIF1 -? exhibit midkine modulating activity. The invention pertains to the discovery that midkine modulates myocardin activity.

Abstract: The present invention provides for a method of treating pulmonary disease in a subject comprising the administration to a subject in need of such treatment a therapeutically effective amount of a formulation comprising a SP-C therapeutic. Preferably, the SP-C therapeutic is an agent selected from the group consisting of an isolated SP-C protein, an isolated nucleic acid molecule encoding a SP-C protein, a SP-C receptor-specific antibody that stimulates the activity of the receptor, or pharmaceutically acceptable composition thereof. The present invention also provides methods of producing a mouse with a targeted disruption in a surfactant protein C (SP-C) gene. The present invention also provides for a transgenic mouse produced by a targeted disruption in a surfactant protein C (SP-C) gene. The present invention further provides for a cell or cell line from a transgenic mouse produced by a targeted disruption in a surfactant protein C (SP-C) gene.

Abstract: Surfactant protein D (SP-D) is a 43-kDa member of the collectin family of collagenous lectin domain-containing proteins that is expressed in epithelial cells of the lung. The SP-D gene was targeted by homologous recombination in embryonic stem cells that were used to produce SP-D (?/?) mice. The SP-D (?/?) deficiency caused inflammation, increased oxidant production by isolated alveolar macrophages, abnormal surfactant structure and levels, and decreased SP-A expression. Therefore, disclosed is the SP-D (?/?) mouse as an excellent model for emphysema. Also included are models for testing emphysema therapies in the mouse model, methods for using SP-D protein or DNA as a treatment for emphysema and pulmonary infections, and diagnosis.

Abstract: Surfactant protein D (SP-D) is a 43-kDa member of the collectin family of collagenous lectin domain-containing proteins that is expressed in epithelial cells of the lung. The SP-D gene was targeted by homologous recombination in embryonic stem cells that were used to produce SP-D (−/−) mice. The SP-D (−/−) deficiency caused inflammation, increased oxidant production by isolated alveolar macrophages, abnormal surfactant structure and levels, and decreased SP-A expression. Therefore, disclosed is the SP-D (−/−) mouse as an excellent model for emphysema. Also included are models for testing emphysema therapies in the mouse model, methods for using SP-D protein or DNA as a treatment for emphysema and pulmonary infections, and diagnosis.

Abstract: Surfactant protein D (SP-D) is a 43-kDa member of the collectin family of collagenous lectin domain-containing proteins that is expressed in epithelial cells of the lung. The SP-D gene was targeted by homologous recombination in embryonic stem cells that were used to produce SP-D (−/−) mice. The SP-D (−/−) deficiency caused inflammation, increased oxidant production by isolated alveolar macrophages, abnormal surfactant structure and levels, and decreased SP-A expression. Therefore, disclosed is the SP-D (−/−) mouse as an excellent model for emphysema. Also included are models for testing emphysema therapies in the mouse model, methods for using SP-D protein or DNA as a treatment for emphysema and pulmonary infections, and diagnosis.

Abstract: Single nucleotide polymorphisms (SNPs) in the gene encoding surfactant protein C can be used to diagnose interstitial lung disease and to determine whether an individual is predisposed to developing interstitial lung disease. Single-stranded polynucleotides comprising a contiguous series of nucleotides from a mutant allele of a surfactant protein C gene, as well as antibodies which specifically bind to altered forms of surfactant protein C but not to wild-type surfactant protein C, can be used in various methods to detect the presence of disease-associated SNPs.

Abstract: An oligonucleotide which includes at least one nucleic acid sequence which binds to at least one nuclear protein found in lung cells, such as TTF-1 protein. The oligonucleotide may be contained in a vector. The at least one nuclear protein provides for lung cell-specific expression of the vector upon binding of the at least one nucleic acid sequence to the at least one nuclear protein. Such vector may also include genes encoding therapeutic agents, and may be employed for delivering genes encoding therapeutic agents to lung cells.

Abstract: An oligonucleotide which includes at least one nucleic acid sequence which binds to at least one nuclear protein found in lung cells, such as TTF-1 protein. The oligonucleotide may be contained in a vector. The at least one nuclear protein provides for lung cell-specific expression of the vector upon binding of the at least one nucleic acid sequence to the at least one nuclear protein. Such vector may also include genes encoding therapeutic agents, and may be employed for delivering genes encoding therapeutic agents to lung cells.

Abstract: A novel hydrophobic surfactant-associated protein mixture, i.e., a SAP-6 proteins, has been isolated from pulmonary animal tissue. A small, novel pulmonary hydrophobic surfactant-associated SAP-6-Val protein having a molecular weight of about 6,000 daltons as determined by SDS-PAGE and about 3,500-4,000 daltons as determined by tricine-SDS-PAGE has been further isolated from the SAP-6 protein mixture. The amino acid residue compositions of the SAP-6-Val protein for human and bovine have been determined and disclosed. When a SAP-6-Val protein is combined with phospholipids, it enhances the surfactant-like activity of the phospholipids in lungs of animals and, therefore, uniquely imparts to the mixture significant pulmonary biophysical activity. Such a mixture results in enhanced adsorption of the phospholipids with properties similar to that of natural pulmonary surfactant material.

Abstract: A novel hydrophobic surfactant-associated protein mixture, i.e., a SAP-6 proteins, has been isolated from pulmonary animal tissue. A small, novel pulmonary hydrophobic surfactant-associated SAP-6-Val protein having a molecular weight of about 6,000 daltons as determined by SDS-PAGE and about 3,500-4,000 daltons as determined by tricine-SDS-PAGE has been further isolated from the SAP-6 protein mixture. The amino acid residue compositions of the SAP-6-Val protein for human and bovine have been determined and disclosed. When a SAP-6-Val protein is combined with phospholipids, it enhances the surfactant-like activity of the phospholipids in lungs of animals and, therefore, uniquely imparts to the mixture significant pulmonary biophysical activity. Such a mixture results in enhanced adsorption of the phospholipids with properties similar to that of natural pulmonary surfactant material.