Literature DB >> 2200279

Clearance and recycling of pulmonary surfactant.

J R Wright1.   

Abstract

In a steady state the rate of secretion of pulmonary surfactant lipids and proteins into the alveolar airspace must be balanced by the rate of removal. Several potential pathways for clearance have been identified including uptake by alveolar type II cells, which also synthesize and secrete surfactant components, uptake by other epithelial cells, and internalization by alveolar macrophages. A small amount of surfactant moves up the airways and through the epithelium-endothelium barrier into the blood. Some of the surfactant lipids and proteins that are cleared from the alveolar airspace appear to be "recycled" in that they appear in the lamellar body, a surfactant secretory granule found in the type II cell. Some surfactant lipids are degraded, probably intracellularly, and the degradation products are reutilized to synthesize new lipids. Several factors have been shown to affect internalization by the type II cell and/or alveolar clearance including the surfactant proteins, lipids, and known stimuli of surfactant secretion. Surfactant proteins may be involved in regulating pool size by modulating both secretion rates and uptake rates, possibly by a receptor-mediated process, although such receptors have not yet been identified or isolated. Clearance of surfactant lipids from the alveolar airspace is more rapid than clearance from the whole lung, and these two processes may be regulated by different factors. Elucidation of the factors that fine tune the balance between synthesis, secretion, and clearance of the lipid and protein components of surfactant awaits further investigation.

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Year:  1990        PMID: 2200279     DOI: 10.1152/ajplung.1990.259.2.L1

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


  25 in total

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Review 3.  The molecular basis of pulmonary alveolar proteinosis.

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4.  Physicochemical effects enhance surfactant transport in pulsatile motion of a semi-infinite bubble.

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5.  Pulmonary delivery of free and liposomal insulin.

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Journal:  Pharm Res       Date:  1993-02       Impact factor: 4.200

6.  Patient-derived granulocyte/macrophage colony-stimulating factor autoantibodies reproduce pulmonary alveolar proteinosis in nonhuman primates.

Authors:  Takuro Sakagami; David Beck; Kanji Uchida; Takuji Suzuki; Brenna C Carey; Koh Nakata; Gary Keller; Robert E Wood; Susan E Wert; Machiko Ikegami; Jeffrey A Whitsett; Maurizio Luisetti; Stella Davies; Jeffrey P Krischer; Alan Brody; Fred Ryckman; Bruce C Trapnell
Journal:  Am J Respir Crit Care Med       Date:  2010-03-11       Impact factor: 21.405

7.  Cross-talk between remodeling and de novo pathways maintains phospholipid balance through ubiquitination.

Authors:  Phillip L Butler; Rama K Mallampalli
Journal:  J Biol Chem       Date:  2009-12-15       Impact factor: 5.157

Review 8.  Eosinophil-associated lung diseases. A cry for surfactant proteins A and D help?

Authors:  Julie G Ledford; Kenneth J Addison; Matthew W Foster; Loretta G Que
Journal:  Am J Respir Cell Mol Biol       Date:  2014-11       Impact factor: 6.914

9.  Fatty acid composition of lung, macrophage and surfactant phospholipids after short-term enteral feeding with n-3 lipids.

Authors:  J D Palombo; E E Lydon; P L Chen; B R Bistrian; R A Forse
Journal:  Lipids       Date:  1994-09       Impact factor: 1.880

10.  Integrin beta6 mediates phospholipid and collectin homeostasis by activation of latent TGF-beta1.

Authors:  Laura L Koth; Byron Alex; Samuel Hawgood; Michael A Nead; Dean Sheppard; David J Erle; David G Morris
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