Control of pulmonary surfactant secretion: an evolutionary perspective

2000 ◽  
Vol 278 (3) ◽  
pp. R611-R619 ◽  
Author(s):  
Philip G. Wood ◽  
Olga V. Lopatko ◽  
Sandra Orgeig ◽  
Jean M. P. Joss ◽  
Allan W. Smits ◽  
...  
Keyword(s):  
Nervous System ◽  
Cell Cultures ◽  
Pulmonary Surfactant ◽  
Parasympathetic Nervous System ◽  
Type Ii Cells ◽  
Type Ii ◽  
Surfactant System ◽  
Surfactant Secretion ◽  
Type Ii Cell ◽  
Australian Lungfish

Pulmonary surfactant, a mixture consisting of phospholipids (PL) and proteins, is secreted by type II cells in the lungs of all air-breathing vertebrates. Virtually nothing is known about the factors that control the secretion of pulmonary surfactant in nonmammalian vertebrates. With the use of type II cell cultures from Australian lungfish, North American bullfrogs, and fat-tailed dunnarts, we describe the autonomic regulation of surfactant secretion among the vertebrates. ACh, but not epinephrine (Epi), stimulated total PL and disaturated PL (DSP) secretion from type II cells isolated from Australian lungfish. Both Epi and ACh stimulated PL and DSP secretion from type II cells of bullfrogs and fat-tailed dunnarts. Neither Epi nor ACh affected the secretion of cholesterol from type II cell cultures of bullfrogs or dunnarts. Pulmonary surfactant secretion may be predominantly controlled by the autonomic nervous system in nonmammalian vertebrates. The parasympathetic nervous system may predominate at lower body temperatures, stimulating surfactant secretion without elevating metabolic rate. Adrenergic influences on the surfactant system may have developed subsequent to the radiation of the tetrapods. Furthermore, ventilatory influences on the surfactant system may have arisen at the time of the evolution of the mammalian bronchoalveolar lung. Further studies using other carefully chosen species from each of the vertebrate groups are required to confirm this hypothesis.

Control of pulmonary surfactant secretion from type II pneumocytes isolated from the lizardPogona vitticeps

1999 ◽  
Vol 277 (6) ◽  
pp. R1705-R1711 ◽  
Author(s):  
Philip G. Wood ◽  
Olga V. Lopatko ◽  
Sandra Orgeig ◽  
Jonathan R. Codd ◽  
Christopher B. Daniels
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Pulmonary Surfactant ◽  
Parasympathetic Nervous System ◽  
Work Of Breathing ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type Ii Pneumocytes ◽  
Surfactant Secretion ◽  
Sympathetic Nervous

Pulmonary surfactant, a mixture consisting of lipids and proteins and secreted by type II cells, functions to reduce the surface tension of the fluid lining of the lung, and thereby decreases the work of breathing. In mammals, surfactant secretion appears to be influenced primarily by the sympathetic nervous system and changes in ventilatory pattern. The parasympathetic nervous system is not believed to affect surfactant secretion in mammals. Very little is known about the factors that control surfactant secretion in nonmammalian vertebrates. Here, a new methodology for the isolation and culture of type II pneumocytes from the lizard Pogona vitticeps is presented. We examined the effects of the major autonomic neurotransmitters, epinephrine (Epi) and ACh, on total phospholipid (PL), disaturated PL (DSP), and cholesterol (Chol) secretion. At 37°C, only Epi stimulated secretion of total PL and DSP from primary cultures of lizard type II cells, and secretion was blocked by the β-adrenoreceptor antagonist propranolol. Neither of the agonists affected Chol secretion. At 18°C, Epi and ACh both stimulated DSP and PL secretion but not Chol secretion. The secretion of surfactant Chol does not appear to be under autonomic control. It appears that the secretion of surfactant PL is predominantly controlled by the autonomic nervous system in lizards. The sympathetic nervous system may control surfactant secretion at high temperatures, whereas the parasympathetic nervous system may predominate at lower body temperatures, stimulating surfactant secretion without elevating metabolic rate.

Effect of secretagogues on cytoplasmic free calcium in alveolar type II epithelial cells

1987 ◽  
Vol 253 (5) ◽  
pp. C679-C686 ◽  
Author(s):  
K. Sano ◽  
D. R. Voelker ◽  
R. J. Mason
Keyword(s):  
Pulmonary Surfactant ◽  
Calcium Concentration ◽  
Free Calcium ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Surfactant Secretion ◽  
Free Calcium Concentration ◽  
Cytoplasmic Free Calcium

Pulmonary surfactant is synthesized and secreted by alveolar type II epithelial cells. Although intracellular calcium and other second messengers have been implicated in secretion by type II cells, this is the first report on measurement of cytoplasmic free calcium concentration ([Ca2+]i). Known secretagogues, 12-O-tetradecanoylphorbol-13-acetate (TPA) and terbutaline, were tested to see if they caused rapid increases in cytoplasmic calcium. Ionomycin, a calcium ionophore, was used to increase cytoplasmic free calcium concentration, to determine if a rapid increase in cytoplasmic free calcium would stimulate secretion, and to measure interactions with other secretagogues. Ionomycin increased both [Ca2+]i and pulmonary surfactant secretion from alveolar type II cells. A low concentration of ionomycin (100 nM) greatly enhanced secretion stimulated by terbutaline or by 8-bromo-cAMP but only had an additive effect on secretion stimulated by TPA. Terbutaline transiently increased [Ca2+]i by 24% over control basal condition, and the increase in [Ca2+]i produced by terbutaline occurred in the absence of extracellular calcium. TPA itself did not change [Ca2+]i. However, TPA completely inhibited the terbutaline-induced increase of [Ca2+]i but not the increase due to ionomycin. When alveolar type II cells were loaded with 2-(2-bis-[carboxymethyl]-amino-5-methyl-phenoxy)-methyl-6-methoxy-8-bis carboxymethylaminoquinoline (quin2) in calcium-free buffer, [Ca2+]i decreased from 143 +/- 10 to 31 +/- 8 nM. Lowering [Ca2+]i inhibited TPA- or terbutaline-induced secretion by 22 and 40%, respectively. Although the precise role of cytoplasmic free calcium on surfactant secretion cannot be established on the basis of current data, our results indicate that an increase in cytoplasmic free calcium produced by ionomycin stimulates secretion and that an increase in [Ca2+]i affects cAMP-induced secretion more than protein kinase C-mediated secretion in alveolar type II cells.

Phosphatidate phosphohydrolase activity as a marker for surfactant synthesis in organotypic cultures of type II alveolar pneumonocytes

1983 ◽  
Vol 60 (1) ◽  
pp. 199-207
Author(s):  
W.H. Douglas ◽  
S.K. Sommers-Smith ◽  
J.M. Johnston
Keyword(s):  
Pulmonary Surfactant ◽  
Specific Activity ◽  
Type Ii Cells ◽  
Type Ii ◽  
Rat Lung ◽  
Organotypic Cultures ◽  
Foetal Rat ◽  
Phosphatidate Phosphohydrolase ◽  
Type Ii Cell ◽  
Specific Activities

The specific activity of phosphatidate phosphohydrolase (PAPase) (EC 3.1.3.4) has been assayed in organotypic cultures of foetal rat lung type II alveolar pneumonocytes and in L2 cells derived from type II cells of the adult rat lung. This enzyme catalyses a critical step in the synthesis of phosphatidylcholine, the major lipid component of pulmonary surfactant. Surfactant is produced by the mature type II cell in culture as well as in vivo. The specific activity of PAPase in organotypic cultures prepared from foetal rat lung starting at 16 days of gestation increased four- to fivefold during the first 7 days in culture. The specific activity of this enzyme was further increased through the 21 days of culture. In parallel with the increase in PAPase specific activity in the cultures were morphological changes in the type II cells such as the appearance of increased numbers of lamellar bodies. The specific activities of PAPase samples derived from non-type II cell cultures maintained under identical conditions were compared. Organotypic cultures and L2 cells, a culture system that also exhibits type II cell characteristics, show PAPase specific activities five to six times greater than cultures that do not contain type II cells. PAPase activity in the type II cell cultures parallels the development of mature patterns of pulmonary surfactant synthesis storage and secretion.

Insulin acts on the fibroblast to inhibit glucocorticoid stimulation of lung maturation

1984 ◽  
Vol 57 (5) ◽  
pp. 1577-1579 ◽  
Author(s):  
K. S. Carlson ◽  
B. T. Smith ◽  
M. Post
Keyword(s):  
Cell Cultures ◽  
Fetal Lung ◽  
Conditioned Media ◽  
Lung Fibroblasts ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lung Maturation ◽  
Mixed Cell ◽  
Type Ii Cell ◽  
Phosphatidylcholine Synthesis

The effects of insulin and cortisol on saturated phosphatidylcholine synthesis are examined in fetal type II cell cultures and in mixed cell cultures containing type II cells and fibroblasts. In 19-day fetal rat lung type II cell cultures, 100 nM cortisol and 2 nM insulin have no significant effect. Fibroblast-pneumonocyte factor results in enhanced saturated phosphatidylcholine synthesis by fetal type II cells. The significant stimulatory effect of cortisol in mixed-cell cultures is abolished in the presence of insulin or of monoclonal antibodies to fibroblast-pneumonocyte factor. Incubation of type II cells with conditioned media from fibroblasts exposed to cortisol results in increased saturated phosphatidylcholine synthesis. This process is not stimulated when type II cells are incubated with conditioned media from fibroblasts exposed to insulin and cortisol (or to insulin alone). These observations demonstrate that insulin inhibits cortisol induction of lung maturation and suggest that this antagonism results from an inhibitory effect of insulin on the elaboration of fibroblast-pneumonocyte factor by fetal lung fibroblasts.

scholarly journals Postnatal development and control of the pulmonary surfactant system in the tammar wallaby Macropus eugenii

2001 ◽  
Vol 204 (23) ◽  
pp. 4031-4042
Author(s):  
Natalie J. Miller ◽  
Sandra Orgeig ◽  
Christopher B. Daniels ◽  
Russell V. Baudinette
Keyword(s):  
Gas Exchange ◽  
Pulmonary Surfactant ◽  
Tammar Wallaby ◽  
Surfactant Proteins ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Macropus Eugenii ◽  
Surfactant System

SUMMARY Marsupials are born at an early stage of development and are adapted for future development inside the pouch. Whether the pulmonary surfactant system is fully established at this altricial stage is unknown. This study correlates the presence of surfactant proteins (SP-A, SP-B and SP-D), using immunohistochemistry, with the ex-utero development of the lung in the tammar wallaby Macropus eugenii and also investigates the control of phosphatidylcholine (PC) secretion from developing alveolar type II cells. All three surfactant proteins were found at the site of gas exchange in the lungs of joeys at all ages, even at birth when the lungs are in the early stages of the terminal air-sac phase. Co-cultures of alveolar type II cells and fibroblasts were isolated from the lungs of 30- and 70-day-old joeys and incubated with the hormones dexamethasone (10 μmol l–1), prolactin (1 μmol l–1) or triiodothyronine (100 μmol l–1) or with the autonomic secretagogues isoproterenol (100 μmol l–1) or carbamylcholine chloride (100 μmol l–1). Basal secretion of PC was greater at 30 days of age than at 70 days. Co-cultures responded to all five agonists at 30 days of age, but only the autonomic secretagogues caused a significant increase in PC secretion at 70 days of age. This demonstrates that, as the cells mature, their activity and responsiveness are reduced. The presence of the surfactant proteins at the site of gas exchange at birth suggests that the system is fully functional. It appears that surfactant development is coupled with the terminal air-sac phase of lung development rather than with birth, the length of gestation or the onset of air-breathing.

Altered lung surfactant system in a Rab38-deficient rat model of Hermansky-Pudlak syndrome

2010 ◽  
Vol 298 (2) ◽  
pp. L243-L251 ◽  
Author(s):  
Kazuhiro Osanai ◽  
Junko Higuchi ◽  
Rieko Oikawa ◽  
Makoto Kobayashi ◽  
Katsuma Tsuchihara ◽  
...  
Keyword(s):  
Interstitial Pneumonia ◽  
Rat Model ◽  
Lung Surfactant ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lamellar Bodies ◽  
Surfactant System ◽  
Surfactant Secretion ◽  
Hermansky Pudlak Syndrome ◽  
Long Evans

Several Long-Evans rat substrains carrying the phenotype of oculocutaneous albinism and bleeding diathesis are a rat model of Hermansky-Pudlak syndrome (HPS). The mutation responsible for the phenotype ( Ruby) was identified as a point mutation in the initiation codon of Rab38 small GTPase that regulates intracellular vesicle transport. As patients with HPS often develop life-limiting interstitial pneumonia accompanied by abnormal morphology of alveolar type II cells, we investigated lung surfactant system in Long-Evans Cinnamon rats, one strain of the Ruby rats. The lungs showed conspicuous morphology of type II cells containing markedly enlarged lamellar bodies. Surfactant phosphatidylcholine and surfactant protein B were increased in lung tissues and lamellar bodies but not in alveolar lumen. Expression levels of mRNA for surfactant proteins A, B, C, and D were not altered. Isolated type II cells showed aberrant secretory pattern of newly synthesized [3H]phosphatidylcholine, i.e., decreased basal secretion and remarkably amplified agonist-induced secretion. [3H]phosphatidylcholine synthesis and uptake by type II cells were not altered. Thus Rab38-deficient type II cells appear to carry abnormality in lung surfactant secretion but not in synthesis or uptake. These results suggest that aberrant lung surfactant secretion may be involved in the pathogenesis of interstitial pneumonia in HPS.

Pulmonary surfactant secretion in briefly cultured mouse type II cells

2004 ◽  
Vol 286 (2) ◽  
pp. L331-L336 ◽  
Author(s):  
Laurice I. Gobran ◽  
Seamus A. Rooney
Keyword(s):  
Adrenergic Receptor ◽  
Pulmonary Surfactant ◽  
Surfactant Protein ◽  
Suitable Model ◽  
Type Ii Cells ◽  
Type Ii ◽  
Surfactant Secretion ◽  
Phosphatidylcholine Secretion

There is little information on the regulation of surfactant secretion in mouse type II cells. We isolated type II cells from C57BL/6 and FVB mice, cultured them overnight, and then examined their response to known surfactant secretagogues. Secretion of phosphatidylcholine, surfactant protein (SP)-B and SP-C was stimulated by terbutaline, 5′- N-ethylcarboxyamidoadenosine (NECA), ATP, UTP, TPA, and ionomycin. Phosphatidylcholine secretion was increased approximately twofold by all agonists in both strains of mice. The response to terbutaline and NECA is the same as in rat type II cells, whereas the response to ATP, UTP, TPA, and ionomycin is considerably less. Secretion of SP-B and SP-C was increased sevenfold by terbutaline and threefold by ATP, effects similar to those in rat type II cells. The response to terbutaline was significantly decreased in type II cells from β2-adrenergic receptor null mice. These data establish that briefly cultured type II cells provide a suitable model for investigation of surfactant secretion in normal and genetically altered mice.

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