Influence of Lung Surfactant Phospholipids on Neutrophilic Granulocytes and Blood Monocytes1

2015 ◽  
pp. 44-50 ◽  
Author(s):  
Connie Jarstrand ◽  
Per Berggren ◽  
Tore Curstedt ◽  
Anne Johansson ◽  
Bengt Robertson ◽  
...  
Keyword(s):  
Lung Surfactant ◽  
Neutrophilic Granulocytes ◽  
Surfactant Phospholipids

scholarly journals Species pattern of phosphatidylinositol from lung surfactant and a comparison of the species pattern of phosphatidylinositol and phosphatidylglycerol synthesized de novo in lung microsomal fractions

1988 ◽  
Vol 254 (1) ◽  
pp. 67-71 ◽  
Author(s):  
B Rüstow ◽  
Y Nakagawa ◽  
H Rabe ◽  
K Waku ◽  
D Kunze
Keyword(s):  
Lung Function ◽  
Molecular Species ◽  
De Novo ◽  
Lung Surfactant ◽  
Minor Component ◽  
Main Species ◽  
Surfactant Phospholipids ◽  
Species Pattern ◽  
A Minor

1. Phosphatidylinositol (PI) is a minor component of lung surfactant which may be able to replace the functionally important phosphatidylglycerol (PG) [Beppu, Clements & Goerke (1983) J. Appl. Physiol. 55, 496-502] without disturbing lung function. The dipalmitoyl species is one of the main species for both PI (14.4%) and PG (16.9%). Besides the C16:0--C16:0 species, the C16:0--C18:0, C16:0--C18:1, C16:0--C18:2 and C18:0--C18:1 species showed comparable proportions in the PG and PI fractions. These similarities of the species patterns and the acidic character of both phospholipids could explain why surfactant PG may be replaced by PI. 2. PI and PG were radiolabelled by incubation of microsomal fractions with [14C]glycerol 3-phosphate (Gro3P). For 11 out of 14 molecular species of PI and PG we measured comparable proportions of radioactivity. The radioactivity of these 11 species accounted together for more than 80% of the total. The addition of inositol to the incubation system decreased the incorporation in vitro of Gro3P into PG and CDP-DG (diacylglycerol) of lung microsomes (microsomal fractions), but did not change the distribution of radioactivity among the molecular species of PG. These results supported the idea that both acidic surfactant phospholipids may be synthesized de novo from a common CDP-DG pool in lung microsomes.

Lung surfactant phospholipids inhibit the uptake of respirable microspheres by the alveolar macrophage NR8383

2002 ◽  
Vol 54 (8) ◽  
pp. 1065-1072 ◽  
Author(s):  
B. G. Jones ◽  
P. A. Dickinson ◽  
M. Gumbleton ◽  
I. W. Kellaway
Keyword(s):  
Alveolar Macrophage ◽  
Lung Surfactant ◽  
Surfactant Phospholipids

Introduction: Lung Surfactant—Phospholipids and Apoproteins

1984 ◽  
Vol 6 (3-4) ◽  
pp. 171-174 ◽  
Author(s):  
Aron B. Fisher ◽  
Avinash Chander
Keyword(s):  
Lung Surfactant ◽  
Surfactant Phospholipids

scholarly journals Effect of triiodothyronine augmentation on rat lung surfactant phospholipids during sepsis

1997 ◽  
Vol 82 (6) ◽  
pp. 2020-2027 ◽  
Author(s):  
Sergey M. Ksenzenko ◽  
Scott B. Davidson ◽  
Amer A. Saba ◽  
Alexander P. Franko ◽  
Aml M. Raafat ◽  
...  
Keyword(s):  
Lung Surfactant ◽  
Cecal Ligation ◽  
Active Role ◽  
Lung Compliance ◽  
Rat Lung ◽  
Sprague Dawley ◽  
Surfactant Phospholipids ◽  
Surfactant Composition ◽  
And Function

Ksenzenko, Sergey M., Scott B. Davidson, Amer A. Saba, Alexander P. Franko, Aml M. Raafat, Lawrence N. Diebel, and Scott A. Dulchavsky. Effect of triiodothyronine augmentation on rat lung surfactant phospholipids during sepsis. J. Appl. Physiol. 82(6): 2020–2027, 1997.—Surfactant functional effectiveness is dependent on phospholipid compositional integrity; sepsis decreases this through an undefined mechanism. Sepsis-induced hypothyroidism is commensurate and may be related. This study examines the effect of 3,3′,5-triiodo-l-thyronine (T3) supplementation on surfactant composition and function during sepsis. Male Sprague-Dawley rats underwent sham laparotomy (Sham) or cecal ligation and puncture (CLP) with or without T3supplementation [CLP/T3 (3 ng/h)]. After 6, 12, or 24 h, surfactant was obtained by lavage. Function was assessed by a pulsating bubble surfactometer and in vivo compliance studies. Sepsis produced a decrease in surfactant phosphatidylglycerol and phosphatidic acid, with an increase in lesser surface-active lipids phosphatidylserine and phosphatidylinositol. Phosphatidylcholine content was not significantly changed. Sepsis caused an alteration in the fatty acid composition and an increase in saturation in most phospholipids. Hormonal replacement attenuated these changes. Lung compliance and surfactant adsorption were reduced by sepsis and maintained by T3treatment. Thyroid hormone may have an active role in lung functional preservation through maintenance of surfactant homeostasis during sepsis.

Lung Surfactant Phospholipids as Related to Hydration and Choline Status of Fasted Rats

1985 ◽  
Vol 115 (1) ◽  
pp. 85-92 ◽  
Author(s):  
James V. Bruno ◽  
Kathleen E. McMahon ◽  
Philip M. Farrell
Keyword(s):  
Lung Surfactant ◽  
Surfactant Phospholipids ◽  
Fasted Rats

scholarly journals Analysis of Labeling and Clearance of Lung Surfactant Phospholipids in Rabbit

1981 ◽  
Vol 68 (3) ◽  
pp. 742-751 ◽  
Author(s):  
Mikko Hallman ◽  
Benita L. Epstein ◽  
Louis Gluck
Keyword(s):  
Lung Surfactant ◽  
Surfactant Phospholipids

Abnormal Lung Surfactant Related to Essential Fatty Acid Deficiency in a Neonate

PEDIATRICS ◽  
1979 ◽  
Vol 63 (6) ◽  
pp. 855-859
Author(s):  
Zvi Friedman ◽  
Abraham Rosenberg
Keyword(s):  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Essential Fatty Acid ◽  
Acid Composition ◽  
Pulmonary Surfactant ◽  
Lung Surfactant ◽  
Fatty Acid Pattern ◽  
Hyaline Membrane Disease ◽  
Lavage Fluid ◽  
Surfactant Phospholipids

A low-birth-weight infant, suffering from chronic bronchopulmonary dysplasia following hyaline membrane disease and recurrent episodes of necrotizing enterocolitis, developed biochemical evidence of essential fatty acid (EFA) deficiency in the plasma. Fatty acid composition of phosphatidylcholine and phosphatidylglycerol in the lung lavage fluid was abnormal. Plasma changes includcd a decrease in the level of linoleic acid and an increased level of palmitic, palmitoleic, oleic, and 5,8, 11-eicosatrienoic acids, the ratio of 5,8,11-eicosatrienoic acid to arachidonic acid being > 0.4:1. A lower than normal level of palmitic acid and an increased level of palmitoleic and oleic acids were seen in pulmonary surfactant phospholipid components. Upon treatment and recovery from EFA deficiency, the fatty acid pattern both in plasma and surfactant phospholipids returned to normal along with clinical improvement. An association between EFA deficiency and altered fatty acid composition of pulmonary surfactant phospholipids is suggested.

Altered fatty acid composition of lung surfactant phospholipids in interstitial lung disease

2002 ◽  
Vol 283 (5) ◽  
pp. L1079-L1085 ◽  
Author(s):  
R. Schmidt ◽  
U. Meier ◽  
P. Markart ◽  
F. Grimminger ◽  
H. G. Velcovsky ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Interstitial Lung Disease ◽  
Palmitic Acid ◽  
Lung Disease ◽  
Pulmonary Surfactant ◽  
Hypersensitivity Pneumonitis ◽  
Lung Surfactant ◽  
Relative Content ◽  
Surfactant Aggregates ◽  
Surfactant Phospholipids

Deterioration of pulmonary surfactant function has been reported in interstitial lung disease; however, the molecular basis is presently unclear. We analyzed fatty acid (FA) profiles of several surfactant phospholipid classes isolated from large-surfactant aggregates of patients with idiopathic pulmonary fibrosis (IPF; n = 12), hypersensitivity pneumonitis ( n = 5), and sarcoidosis ( n = 12). Eight healthy individuals served as controls. The relative content of palmitic acid in phosphatidylcholine was significantly reduced in IPF (66.8 ± 2.5%; means ± SE; P < 0.01) but not in hypersensitivity pneumonitis (78.5 ± 1.8%) and sarcoidosis (78.2 ± 3.1%; control 80.1 ± 0.7%). In addition, the phosphatidylglycerol FA profile was significantly altered in the IPF patients, with a lower relative content of its major FA, oleic acid, at the expense of saturated FA. In the phosphatidylcholine class, a significant correlation between the impairment of biophysical surfactant function and decreased percentages of palmitic acid was noted. We conclude that significant alterations in the FA profile of pulmonary surfactant phospholipids occur predominantly in IPF and may contribute to the disturbances of alveolar surface activity in this disease.

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