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Pulmonary surfactant is a surface-active complex of phospholipids and proteins formed by type II alveolar cells. [1] The proteins and lipids that make up the surfactant have both hydrophilic and hydrophobic regions.
Surfactant therapy is the medical administration of pulmonary surfactant that is derived from outside of the body. Pulmonary surfactant is a soap-like chemical synthesized by type II alveolar pneumocytes and is of various lipids (80% phospholipids, 5-10% cholesterol, and ∼10% surfactant-associated proteins).
Pulmonary surfactant is used as a medication to treat and prevent respiratory distress syndrome in newborn babies. [ 1 ] Prevention is generally done in babies born at a gestational age of less than 32 weeks. [ 1 ]
Dipalmitoylphosphatidylcholine (DPPC) is a phospholipid (and a lecithin) consisting of two C 16 palmitic acid groups attached to a phosphatidylcholine head-group.. It is the main constituent of pulmonary surfactants, which reduces the work of breathing and prevents alveolar collapse during breathing.
Surfactant metabolism dysfunction is a condition where pulmonary surfactant is insufficient for adequate respiration. Surface tension at the liquid-air interphase in the alveoli makes the air sacs prone to collapsing post expiration. This is due to the fact that water molecules in the liquid-air surface of alveoli are more attracted to one ...
The protein component of surfactant helps in the modulation of the innate immune response, and inflammatory processes. Alveolar sac region of the lung - TEM. SP-A1 is a member of a subfamily of C-type lectins called collectins. Together with SP-A2, they are the most abundant proteins of pulmonary surfactant.
The protein component of surfactant helps in the modulation of the innate immune response, and inflammatory processes. [7] Alveolar sac region of the lung - TEM. SP-A2 is a member of a subfamily of C-type lectins called collectins. Together with (surfactant protein A1 ) SP-A1, they are the most abundant proteins of pulmonary surfactant.
The propeptide of pulmonary surfactant C has an N-terminal alpha-helical segment whose suggested function was stabilization of the protein structure, since the mature peptide can irreversibly transform from its native alpha-helical structure to beta-sheet aggregates and form amyloid fibrils. The correct intracellular trafficking of proSP-C has ...