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Surfactant protein A (SP-A) gene targeted mice
T R Korfhagen1, A M LeVine, J A Whitsett
1Division of Pulmonary Biology, Children's Hospital Research Foundation, 3333 Burnet Avenue, Cincinnati, Ohio 45229-3039, USA.
Biochimica Et Biophysica Acta
|November 14, 1998
Summary
Mice without surfactant protein A (SP-A) show impaired lung immunity. These mice are less effective at clearing bacteria, highlighting SP-A's crucial role in the innate immune system.
Area of Science:
- Pulmonary immunology
- Molecular biology
- Genetics
Background:
- Surfactant protein A (SP-A) is a key component of the lung's innate immune system.
- The specific in vivo functions of SP-A, particularly in host defense, require further elucidation.
Purpose of the Study:
- To investigate the role of SP-A in lung immunity and host defense in vivo.
- To characterize the physiological and immunological consequences of SP-A deficiency in mice.
Main Methods:
- Gene targeting was employed to generate mice lacking SP-A (SP-A -/-).
- SP-A (-/-) mice were assessed for survival, breeding, lung phospholipid metabolism, and clearance of bacterial pathogens (Group B streptococci and Pseudomonas aeruginosa).
- Levels of other surfactant proteins (SP-B, SP-C, SP-D) were analyzed.
Main Results:
- SP-A (-/-) mice survived and bred normally, with no alterations in other surfactant proteins or lung phospholipid dynamics.
- A significant reduction in tubular myelin figures was observed in the lungs of SP-A (-/-) mice.
- SP-A (-/-) mice exhibited impaired clearance of Group B streptococci and Pseudomonas aeruginosa compared to wild-type mice.
Conclusions:
- SP-A is not essential for survival, reproduction, or normal lung phospholipid homeostasis.
- SP-A plays a critical role in the innate immune defense of the lung against bacterial pathogens.
- The absence of SP-A leads to reduced tubular myelin and compromised bacterial clearance, underscoring its importance in lung immunity.