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Articoli di riviste sul tema "Pulmonary surfactant"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 25 luglio 2025

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1

van Golde, LMG, JJ Batenburg, and B. Robertson. "The Pulmonary Surfactant System." Physiology 9, no. 1 (1994): 13–20. http://dx.doi.org/10.1152/physiologyonline.1994.9.1.13.

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Abstract (sommario):

The pulmonary surfactant system includes specific proteins involved in the regulation of surfactant secretion and recycling, conversion of secreted lamellar bodies to tubular myelin, film adsorption, and stimulation of alveolar macrophages. Hydrophobic proteins are essential for the rapid physiological action of exogenous surfactants currently used in clinical practice.

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2

Ramanathan, Rangasamy. "Surfactants in the Management of Respiratory Distress Syndrome in Extremely Premature Infants." Journal of Pediatric Pharmacology and Therapeutics 11, no. 3 (2006): 132–44. http://dx.doi.org/10.5863/1551-6776-11.3.132.

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Respiratory distress syndrome (RDS) is primarily due to decreased production of pulmonary surfactant, and it is associated with significant neonatal morbidity and mortality. Exogenous pulmonary surfactant therapy is currently the treatment of choice for RDS, as it demonstrates the best clinical and economic outcomes. Studies confirm the benefits of surfactant therapy to include reductions in mortality, pneumothorax, and pulmonary interstitial emphysema, as well as improvements in oxygenation and an increased rate of survival without bronchopulmonary dysplasia. Phospholipids (PL) and surfactant

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3

Dipak, Kumar Dhar, and Paul Debasish. "Surfactant Replacement Therapy: An Overview." International Journal of Science and Healthcare Research 5, no. 2 (2020): 399–406. https://doi.org/10.5281/zenodo.3931623.

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Abstract (sommario):

Pulmonary surfactant is a soap-like chemical synthesized by type II alveolar pneumocytes and is a mixture of phospholipids (predominantly dipalmitoylphosphatidylcholine), some other lipids and proteins. Its main functions include lowering the surface tension and maintaining the stability of alveoli. The first documented trial involving exogenous use of surfactants as a therapy was recorded in early 1970s using synthetically produced phospholipid mixtures once the chemical composition of surfactants was deciphered. Gradually there was a transition to the use of more natural sources. And animal

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4

Satyam Prakash, Hem Shankar Yadav, and Om Prakash Yadav. "Pulmonary Surfactant in Health and Disease: An Overview." Janaki Medical College Journal of Medical Science 12, no. 03 (2024): 108–22. https://doi.org/10.3126/jmcjms.v12i03.73990.

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Abstract (sommario):

Surfactant is a complex mixture of phospholipids, mainly dipalmitoylphosphatidylcholine (DPCC) and surfactant proteins (SP); SP-A, SP-B, SP-C, and SP-D. DPCC plays a crucial role in lowering the surface tension, while SPs provide immunity against invading pathogens. SPs also enhance the activity of phospholipids, aiding in the adsorption and spread of surfactants all over the alveolar surface. Surfactant production starts as early as 24 weeks of gestation in humans and peaks at about 36-38 weeks. The generation and secretion of lung surfactants are tightly regulated processes. Surfactant is sy

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5

Ignatova, G. L., V. N. Antonov, and I. A. Zakharova. "The use of exogenous surfactant in pulmonological practice." Meditsinskiy sovet = Medical Council, no. 5 (May 9, 2024): 41–48. http://dx.doi.org/10.21518/ms2024-089.

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A lung surfactant is a complex mixture of lipids and proteins necessary to maintain proper lung function. Drug changes play an important role in chronic lung diseases such as chronic obstructive pulmonary disease, bronchial asthma and idiopathic pulmonary fibrosis. The purpose of this article is to substantiate the use of exogenous surfactant in various respiratory diseases, based on the analysis of publications in domestic and international medical journals, as well as their own experience of application in real clinical practice. This review primarily discusses the contribution of pulmonary

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6

Bernhard, Wolfgang, Andreas Gebert, Gertrud Vieten, et al. "Pulmonary surfactant in birds: coping with surface tension in a tubular lung." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 1 (2001): R327—R337. http://dx.doi.org/10.1152/ajpregu.2001.281.1.r327.

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As birds have tubular lungs that do not contain alveoli, avian surfactant predominantly functions to maintain airflow in tubes rather than to prevent alveolar collapse. Consequently, we have evaluated structural, biochemical, and functional parameters of avian surfactant as a model for airway surfactant in the mammalian lung. Surfactant was isolated from duck, chicken, and pig lung lavage fluid by differential centrifugation. Electron microscopy revealed a uniform surfactant layer within the air capillaries of the bird lungs, and there was no tubular myelin in purified avian surfactants. Phosp

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7

Suresh, G. K., and R. F. Soll. "Exogenous Surfactant Therapy in Newborn Infants." Annals of the Academy of Medicine, Singapore 32, no. 3 (2003): 335–45. http://dx.doi.org/10.47102/annals-acadmedsg.v32n3p335.

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Abstract (sommario):

Exogenous surfactant therapy has an established role in the management of neonatal respiratory distress syndrome (RDS). This article summarises the current evidence on surfactant therapy. The use of surfactant for the treatment or prophylaxis of neonatal RDS results in a 30% to 65% relative reduction in the risk of pneumothorax and up to a 40% relative reduction in the risk of mortality. Adverse effects, of which pulmonary haemorrhage is of most concern, are infrequent and long-term follow-up studies of treated patients are reassuring. Natural surfactants have advantages over synthetic surfact

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8

PUTMAN, Esther, Lambert A. J. M. CREUWELS, Lambert M. G. van GOLDE, and Henk P. HAAGSMAN. "Surface properties, morphology and protein composition of pulmonary surfactant subtypes." Biochemical Journal 320, no. 2 (1996): 599–605. http://dx.doi.org/10.1042/bj3200599.

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Separation of surfactant subtypes is now commonly used as a parameter in assessing the amount of active compared with inactive material in various models of lung injury. The protein content, morphology and surface activity were determined of the heavy and light subtype isolated by differential centrifugation. Here we report the presence of surfactant proteins B and C in the heavy subtype but not in the light subtype. Adsorption studies revealed that separation of fast adsorbing bronchoalveolar lavage resulted in slowly adsorbing heavy and light subtypes. Surfactant, reconstituted from heavy an

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9

Dushianthan, Ahilanandan, Michael P. W. Grocott, Ganapathy Senthil Murugan, Tom M. A. Wilkinson, and Anthony D. Postle. "Pulmonary Surfactant in Adult ARDS: Current Perspectives and Future Directions." Diagnostics 13, no. 18 (2023): 2964. http://dx.doi.org/10.3390/diagnostics13182964.

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Acute respiratory distress syndrome (ARDS) is a major cause of hypoxemic respiratory failure in adults, leading to the requirement for mechanical ventilation and poorer outcomes. Dysregulated surfactant metabolism and function are characteristic of ARDS. A combination of alveolar epithelial damage leading to altered surfactant synthesis, secretion, and breakdown with increased functional inhibition from overt alveolar inflammation contributes to the clinical features of poor alveolar compliance and alveolar collapse. Quantitative and qualitative alterations in the bronchoalveolar lavage and tr

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10

Nguyen, Thuy N., Stephanie M. Cunsolo, Peter Gal, and J. Laurence Ransom. "Infasurf and Curosurf: Theoretical and Practical Considerations with New Surfactants." Journal of Pediatric Pharmacology and Therapeutics 8, no. 2 (2003): 97–114. http://dx.doi.org/10.5863/1551-6776-8.2.97.

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Abstract (sommario):

Type II pneumocytes, normally responsible for surfactant production and release, are insufficiently formed and differentiated in the premature infant born before 34 weeks' gestation. Without an adequate amount of pulmonary surfactant, alveolar surface tension increases, leading to collapse and decreased lung compliance. Pulmonary surfactants are naturally occurring substances made of lipids and proteins. They lower surface tension at the interface between the air in the lungs, specifically at the alveoli, and the blood in the capillaries. This review examines the relative benefits of the two m

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11

Dobbs, L. G. "Pulmonary Surfactant." Annual Review of Medicine 40, no. 1 (1989): 431–46. http://dx.doi.org/10.1146/annurev.me.40.020189.002243.

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12

Johansson, Jan, Magnus Gustafsson, Marie Palmblad, Shahparak Zaltash, Bengt Robertson, and Tore Curstedt. "Pulmonary Surfactant." BioDrugs 11, no. 2 (1999): 71–77. http://dx.doi.org/10.2165/00063030-199911020-00001.

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13

Nishijima, Koji, Ken-ichi Shukunami, Hideo Yoshinari, et al. "Interactions among pulmonary surfactant, vernix caseosa, and intestinal enterocytes: intra-amniotic administration of fluorescently liposomes to pregnant rabbits." American Journal of Physiology-Lung Cellular and Molecular Physiology 303, no. 3 (2012): L208—L214. http://dx.doi.org/10.1152/ajplung.00081.2011.

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Abstract (sommario):

Although vernix caseosa is known to be a natural biofilm at birth, human pulmonary surfactant commences to remove the vernix from fetal skin into the amniotic fluid at gestational week 34, i.e., well before delivery. To explain this paradox, we first produced two types of fluorescently labeled liposomes displaying morphology similar to that of pulmonary surfactant and vernix caseosa complexes. We then continuously administered these liposomes into the amniotic fluid space of pregnant rabbits. In addition, we produced pulmonary surfactant and vernix caseosa complexes and administered them into

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14

Rosenberg, O. A. "Pulmonary Surfactant Preparations and Surfactant Therapy for ARDS in Surgical Intensive Care (a Literature Review)." Creative surgery and oncology 9, no. 1 (2019): 50–65. http://dx.doi.org/10.24060/2076-3093-2019-9-1-50-65.

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Introduction. Despite the fact that clinical studies of pulmonary surfactants conducted over many years have demonstrated their efficacy for the treatment of acute respiratory distress syndrome (ARDS) which led to their approval for use inRussia andBelarus, only a few similar positive results have been achieved in other countries. This calls for an extensive literature review for intensive care professionals.Materials and methods. Using the data from 87 papers this review covers the composition, properties, methods of administration and delivery strategies of surfactant in the treatment and pr

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15

Aliouat, EM, R. Escamilla, C. Cariven, et al. "Surfactant changes during experimental pneumocystosis are related to Pneumocystis development." European Respiratory Journal 11, no. 3 (1998): 542–47. http://dx.doi.org/10.1183/09031936.98.11030542.

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Pneumocystosis-related surfactant changes have been reported in both humans and corticosteroid-treated experimental hosts. As corticosteroids induce an increase in pulmonary surfactant, some findings could be considered as controversial. The aim of this study was to investigate whether the surfactant composition changes during experimental pneumocystosis were related to the Pneumocystis development. In this work two corticosteroid-untreated animal models were used: rabbits, which develop spontaneous pneumocystosis at weaning; and severe combined immunodeficiency mice, which were intranasally i

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16

Rahaman, Sk Mehebub, Budhadeb Chowdhury, Animesh Acharjee, Bula Singh, and Bidyut Saha. "Surfactant-based therapy against COVID-19: A review." Tenside Surfactants Detergents 58, no. 6 (2021): 410–15. http://dx.doi.org/10.1515/tsd-2021-2382.

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Abstract The coronavirus disease 2019 (COVID-19) has led to serious health and economic damage to all over the world, and it still remains unstoppable. The SARS-CoV-2, by using its S-glycoprotein, binds with an angiotensin-converting enzyme 2 receptor, mostly present in alveolar epithelial type II cells. Eventually pulmonary surfactant depletion occurs. The pulmonary surfactant is necessary for maintaining the natural immunity as well as the surface tension reduction within the lung alveoli during the expiration. Its insufficiency results in the reduction of blood oxygenation, poor pulmonary r

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17

Kobayashi, T., W. Z. Li, K. Tashiro, et al. "Disparity between tidal and static volumes of immature lungs treated with reconstituted surfactants." Journal of Applied Physiology 80, no. 1 (1996): 62–68. http://dx.doi.org/10.1152/jappl.1996.80.1.62.

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We biologically assessed functions of several reconstituted surfactants with the same minimum surface tension (2-3 mN/m) as “complete” porcine pulmonary surfactant (natural surfactant) but with longer surface adsorption times. Administration of natural surfactant (adsorption time 0.29 s) into the lungs of surfactant-deficient immature rabbits brought a tidal volume of 16.1 +/- 4.4 (SD) ml/kg during mechanical ventilation with 40 breaths/min and 20 cmH2O insufflation pressure. In static pressure-volume recordings, these animals showed a lung volume of 62.4 +/- 9.7 ml/kg at 30 cmH2O airway press

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18

Walther, Frans J., Monik Gupta, Michael M. Lipp, et al. "Aerosol delivery of dry powder synthetic lung surfactant to surfactant-deficient rabbits and preterm lambs on non-invasive respiratory support." Gates Open Research 3 (January 14, 2019): 6. http://dx.doi.org/10.12688/gatesopenres.12899.1.

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Background: The development of synthetic lung surfactant for preterm infants has focused on peptide analogues of native surfactant proteins B and C (SP-B and SP-C). Non-invasive respiratory support with nasal continuous positive airway pressure (nCPAP) may benefit from synthetic surfactant for aerosol delivery. Methods: A total of three dry powder (DP) surfactants, consisting of phospholipids and the SP-B analogue Super Mini-B (SMB), and one negative control DP surfactant without SMB, were produced with the Acorda Therapeutics ARCUS® Pulmonary Dry Powder Technology. Structure of the DP surfact

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19

Walther, Frans J., Monik Gupta, Michael M. Lipp, et al. "Aerosol delivery of dry powder synthetic lung surfactant to surfactant-deficient rabbits and preterm lambs on non-invasive respiratory support." Gates Open Research 3 (March 14, 2019): 6. http://dx.doi.org/10.12688/gatesopenres.12899.2.

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Abstract (sommario):

Background: The development of synthetic lung surfactant for preterm infants has focused on peptide analogues of native surfactant proteins B and C (SP-B and SP-C). Non-invasive respiratory support with nasal continuous positive airway pressure (nCPAP) may benefit from synthetic surfactant for aerosol delivery. Methods: A total of three dry powder (DP) surfactants, consisting of phospholipids and the SP-B analogue Super Mini-B (SMB), and one negative control DP surfactant without SMB, were produced with the Acorda Therapeutics ARCUS® Pulmonary Dry Powder Technology. Structure of the DP surfact

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20

Wright, Jo Rae, and Samuel Hawgood. "Pulmonary Surfactant Metabolism." Clinics in Chest Medicine 10, no. 1 (1989): 83–93. http://dx.doi.org/10.1016/s0272-5231(21)00606-7.

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21

Wood, Alastair J. J., and Alan H. Jobe. "Pulmonary Surfactant Therapy." New England Journal of Medicine 328, no. 12 (1993): 861–68. http://dx.doi.org/10.1056/nejm199303253281208.

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22

LACAZE-MASMONTEIL, THIERRY. "Pulmonary surfactant proteins." Critical Care Medicine 21, Supplement (1993): S376—S378. http://dx.doi.org/10.1097/00003246-199309001-00048.

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23

Kuroki, Y., and D. R. Voelker. "Pulmonary surfactant proteins." Journal of Biological Chemistry 269, no. 42 (1994): 25943–46. http://dx.doi.org/10.1016/s0021-9258(18)47138-4.

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24

SHANNON, DANIEL C. "Pulmonary Surfactant System." Anesthesiology 62, no. 2 (1985): 216. http://dx.doi.org/10.1097/00000542-198502000-00040.

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25

&NA;. "Pulmonary surfactant genetics." Advances in Anatomic Pathology 5, no. 2 (1998): 118. http://dx.doi.org/10.1097/00125480-199803000-00023.

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26

Sherman, M. P., J. B. D'Ambola, E. E. Aeberhard, and C. T. Barrett. "Surfactant therapy of newborn rabbits impairs lung macrophage bactericidal activity." Journal of Applied Physiology 65, no. 1 (1988): 137–45. http://dx.doi.org/10.1152/jappl.1988.65.1.137.

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Abstract (sommario):

Because in vitro studies indicate that pulmonary alveolar macrophages (PAM's) filled with phospholipid vesicles have depressed microbicidal capacity, we tested the intrapulmonary bactericidal activity of newborn PAM's after surfactant treatment. Term newborn rabbits received intratracheally either homologous surfactant or one of two artificial phospholipid vesicle preparations followed by pulmonary aerosol infection with group B streptococci (GBS). Four hours after lung infection, phagocytic killing of GBS was reduced by 70-90% in animals treated with the homologous and one of the artificial s

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27

Kosim, M. Sholeh. "Use of surfactant in neonatal intensive care units." Paediatrica Indonesiana 45, no. 6 (2016): 233. http://dx.doi.org/10.14238/pi45.6.2005.233-40.

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Abstract (sommario):

Surfactant is currently an important therapyfor newborns in neonatal intensive care units(NICUs) with respiratory problems,specifically respiratory distress syndrome(RDS). Surfactant was initially used in 1959, after itwas recognized for maintaining lung inflation at lowtranspulmonary pressures. Avery and Mead in Jobereported that saline extracts from the lungs ofpreterm infants with RDS lacked the low surfacetension characteristics of pulmonary surfactant.Subsequently, in 1980, clinical potential of surfactanttherapy for RDS was demonstrated by Fujiwara et al,reported in Jobe, in the use of s

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28

Soll, Roger F., and Jerold F. Lucey. "Surfactant Replacement Therapy." Pediatrics In Review 12, no. 9 (1991): 261–67. http://dx.doi.org/10.1542/pir.12.9.261.

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Despite medical and technological advances, respiratory distress syndrome (RDS) remains a major cause of morbidity and mortality in premature infants. Thirty years have passed since Avery and Mead demonstrated that infants dying of RDS were deficient in pulmonary surfactant. In those three decades, advances in our understanding of the composition, function, and metabolism of pulmonary surfactant have finally led to clinical trials of surfactant replacement therapy in thousands of premature infants. This article reviews the current status of surfactant replacement therapy. BACKGROUND Pulmonary

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29

Elssner, Andreas, Gertraud Mazur, and Claus Vogelmeier. "Inhibition of factor XIIIa-mediated incorporation of fibronectin into fibrin by pulmonary surfactant." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 4 (1999): L625—L630. http://dx.doi.org/10.1152/ajplung.1999.276.4.l625.

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Intra-alveolar deposition of exudated plasma proteins is a hallmark of acute and chronic inflammatory lung diseases. In particular, fibrin and fibronectin may provide a primary matrix for fibrotic lung remodeling in the alveolar compartment. The present study was undertaken to explore the effect of two surfactant preparations on the incorporation of fibronectin into fibrin. We observed that surfactant phospholipids are associated with insoluble fibrin, factor XIIIa-cross-linked fibrin, and cross-linked fibrin with incorporated fibronectin. Factor XIIIa-mediated binding of fibronectin to fibrin

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30

Gemci, Tevfik, Valery Ponyavin, Richard Collins, Timothy E. Corcoran, Suvash C. Saha, and Mohammad S. Islam. "CFD Study of Dry Pulmonary Surfactant Aerosols Deposition in Upper 17 Generations of Human Respiratory Tract." Atmosphere 13, no. 5 (2022): 726. http://dx.doi.org/10.3390/atmos13050726.

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The efficient generation of high concentrations of fine-particle, pure surfactant aerosols provides the possibility of new, rapid, and effective treatment modalities for Acute Respiratory Distress Syndrome (ARDS). SUPRAER-CATM is a patented technology by Kaer BiotherapeuticsTM, which is a new class of efficient aerosol drug generation and delivery system using Compressor Air (CA). SUPRAER-CA is capable of aerosolizing relatively viscous solutions or suspensions of proteins and surfactants and of delivering them as pure fine particle dry aerosols. In this Computational Fluid Dynamics (CFD) stud

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31

Liu, Lin, and Quanmin Deng. "Profound Effect of Pulmonary Surfactant on the Treatment of Preterm Infants with Respiratory Distress Syndrome." Contrast Media & Molecular Imaging 2022 (October 3, 2022): 1–10. http://dx.doi.org/10.1155/2022/4166994.

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Abstract (sommario):

Inherited diseases caused by dysfunction of pulmonary surfactant metabolism or surfactant dysfunction have recently been considered the underlying causes of neonatal and pediatric respiratory diseases. Respiratory distress syndrome in premature infants is a common respiratory disease in pediatrics. It is caused by underdeveloped lungs in infants and a lack of active substances on the surface of the alveoli, which leads to insufficiency of lung function, which can lead to difficulty breathing, increased heart rate, facial bruising, and more. Neonatal Respiratory Distress Syndrome is a very dang

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32

Milad, Nadia, and Mathieu C. Morissette. "Revisiting the role of pulmonary surfactant in chronic inflammatory lung diseases and environmental exposure." European Respiratory Review 30, no. 162 (2021): 210077. http://dx.doi.org/10.1183/16000617.0077-2021.

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Abstract (sommario):

Pulmonary surfactant is a crucial and dynamic lung structure whose primary functions are to reduce alveolar surface tension and facilitate breathing. Though disruptions in surfactant homeostasis are typically thought of in the context of respiratory distress and premature infants, many lung diseases have been noted to have significant surfactant abnormalities. Nevertheless, preclinical and clinical studies of pulmonary disease too often overlook the potential contribution of surfactant alterations – whether in quantity, quality or composition – to disease pathogenesis and symptoms. In inflamma

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33

Rider, E. D., A. H. Jobe, M. Ikegami, and B. Sun. "Different ventilation strategies alter surfactant responses in preterm rabbits." Journal of Applied Physiology 73, no. 5 (1992): 2089–96. http://dx.doi.org/10.1152/jappl.1992.73.5.2089.

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The effect of ventilation strategy on in vivo function of different surfactants was evaluated in preterm rabbits delivered at 27 days gestational age and ventilated with either 0 cmH2O positive end-expiratory pressure (PEEP) at tidal volumes of 10–11 ml/kg or 3 cmH2O PEEP at tidal volumes of 7–8 ml/kg after treatment with one of four different surfactants: sheep surfactant, the lipids of sheep surfactant stripped of protein (LH-20 lipid), Exosurf, and Survanta. The use of 3 cmH2O PEEP decreased pneumothoraces in all groups except for the sheep surfactant group where pneumothoraces increased (P

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34

Wright, J. R. "Clearance and recycling of pulmonary surfactant." American Journal of Physiology-Lung Cellular and Molecular Physiology 259, no. 2 (1990): L1—L12. http://dx.doi.org/10.1152/ajplung.1990.259.2.l1.

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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

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35

Notter, Robert H., Rohun Gupta, Adrian L. Schwan, Zhengdong Wang, Mohanad Gh Shkoor, and Frans J. Walther. "Synthetic lung surfactants containing SP-B and SP-C peptides plus novel phospholipase-resistant lipids or glycerophospholipids." PeerJ 4 (October 27, 2016): e2635. http://dx.doi.org/10.7717/peerj.2635.

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BackgroundThis study examines the biophysical and preclinical pulmonary activity of synthetic lung surfactants containing novel phospholipase-resistant phosphonolipids or synthetic glycerophospholipids combined with Super Mini-B (S-MB) DATK and/or SP-Css ion-lock 1 peptides that replicate the functional biophysics of surfactant proteins (SP)-B and SP-C. Phospholipase-resistant phosphonolipids used in synthetic surfactants are DEPN-8 and PG-1, molecular analogs of dipalmitoyl phosphatidylcholine (DPPC) and palmitoyl-oleoyl phosphatidylglycerol (POPG), while glycerophospholipids used are active

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Erokhin, V. V., L. N. Lepekha, M. V. Erokhina, I. V. Bocharova, A. V. Kurynina, and G. E. Onishchenko. "SELECTIVE EFFECTS OF PULMONARY SURFACTANT ON VARIOUS SUBPOPULATIONS OF ALVEOLAR MACROPHAGES IN THE MODEL OF EXPERIMENTAL TUBERCULOSIS." Annals of the Russian academy of medical sciences 67, no. 11 (2012): 22–28. http://dx.doi.org/10.15690/vramn.v67i11.467.

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Pulmonary surfactant is necessary component for maintenance of high level of phagocytic activity of alveolar macrophages. Tuberculosis inflammation reduces the production of surfactant by type II cells and phagocytic activity of alveolar macrophages. The effects of exogenous pulmonary surfactant on the ultrastructural changes of various subpopulations of alveolar macrophages were studied by TEM-method. For investigations the bronchial alveolar lavage fluid from guinea pigs infected of M. tuberculosis and treated by isoniazid or isoniazid + exogenous pulmonary surfactant were used. It was shown

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37

Homer, Robert J., Tao Zheng, Geoff Chupp, et al. "Pulmonary type II cell hypertrophy and pulmonary lipoproteinosis are features of chronic IL-13 exposure." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 1 (2002): L52—L59. http://dx.doi.org/10.1152/ajplung.00438.2001.

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Interleukin (IL)-13, a key mediator of Th2-mediated immunity, contributes to the pathogenesis of asthma and other pulmonary diseases via its ability to generate fibrosis, mucus metaplasia, eosinophilic inflammation, and airway hyperresponsiveness. In these studies, we compared surfactant accumulation in wild-type mice and mice in which IL-13 was overexpressed in the lung. When compared with littermate controls, transgenic animals showed alveolar type II cell hypertrophy under light and electron microscopy. Over time, their alveoli also filled with surfactant in a pulmonary alveolar proteinosis

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Whitsett, Jeffrey A. "Review: The intersection of surfactant homeostasis and innate host defense of the lung: lessons from newborn infants." Innate Immunity 16, no. 3 (2010): 138–42. http://dx.doi.org/10.1177/1753425910366879.

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Abstract (sommario):

The study of pulmonary surfactant, directed towards prevention and treatment of respiratory distress syndrome in preterm infants, led to the identification of novel proteins/genes that determine the synthesis, packaging, secretion, function, and catabolism of alveolar surfactant. The surfactant proteins, SP-A, SP-B, SP-C, and SP-D, and the surfactant lipid associated transporter, ABCA3, play critical roles in surfactant homeostasis. The study of their structure and function provided insight into a system that integrates the biophysical need to reduce surface tension in the alveoli and the inna

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Gavrysyuk, V. K., Y. O. Dziublyk, N. A. Vlasova, et al. "PULMONARY ALVEOLAR PROTEINOSIS: THE CASE OF SUBTOTAL PULMONARY PARENCHYMA INVOLVEMENT." Ukrainian Pulmonology Journal 32, no. 1 (2024): 49–58. http://dx.doi.org/10.31215/2306-4927-2024-32-1-49-58.

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Pulmonary alveolar proteinosis (PAP) is a rare pulmonary disease, characterized by the intraalveolar accumulation of surfactant-like lipoprotein substance. There are three forms of the disease: autoimmune (formerly known as idiopathic), secondary and congenital PAP. The disturbances of surfactant metabolism (protein-lipoid complex secreted by type II pneumocytes) play the crucial role in the development of the disease. Surfactant decreases a surface tension of alveoli and prevents its collapse at the end of the expiration and takes part in protection against infections as well. Surfactant is i

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Gross, N. J. "Pulmonary surfactant: unanswered questions." Thorax 50, no. 4 (1995): 325–27. http://dx.doi.org/10.1136/thx.50.4.325.

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Rider, Evelyn. "Metabolism of Pulmonary Surfactant." Seminars in Respiratory and Critical Care Medicine 16, no. 01 (1995): 17–28. http://dx.doi.org/10.1055/s-2007-1009812.

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Caminiti, Stephen P., and Stephen L. Young. "The Pulmonary Surfactant System." Hospital Practice 26, no. 1 (1990): 87–100. http://dx.doi.org/10.1080/21548331.1991.11704128.

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Chroneos, Zissis C., Krishna Midde, Zvjezdana Sever-Chroneos, and Chinnaswamy Jagannath. "Pulmonary surfactant and tuberculosis." Tuberculosis 89 (December 2009): S10—S14. http://dx.doi.org/10.1016/s1472-9792(09)70005-8.

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Weaver, Timothy E. "Pulmonary surfactant-associated proteins." General Pharmacology: The Vascular System 19, no. 3 (1988): 361–68. http://dx.doi.org/10.1016/0306-3623(88)90029-8.

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Orgeig, Sandra, Allan W. Smits, Christopher B. Daniels, and Jay K. Herman. "Surfactant regulates pulmonary fluid balance in reptiles." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 6 (1997): R2013—R2021. http://dx.doi.org/10.1152/ajpregu.1997.273.6.r2013.

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Abstract (sommario):

Reptilian lungs are potentially susceptible to fluid disturbances because they have very high pulmonary fluid filtration rates. In mammals, pulmonary surfactant protects the lung from developing alveolar edema. Reptiles also have an order of magnitude more surfactant per square centimeter of respiratory surface area compared with mammals. We investigated the role of reptilian surfactant 1) in the entry of vascularly derived fluid into the alveolar space of the isolated perfused lizard ( Pogona vitticeps) lung and 2) in the removal of accumulated fluid from the alveolar space of the isolated pe

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Seeger, W., C. Grube, A. Gunther, and R. Schmidt. "Surfactant inhibition by plasma proteins: differential sensitivity of various surfactant preparations." European Respiratory Journal 6, no. 7 (1993): 971–77. http://dx.doi.org/10.1183/09031936.93.06070971.

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Abstract (sommario):

Leakage of plasma proteins into the alveolar space may inhibit surfactant function. We compared the surface properties and the sensitivity to inhibitory proteins of different organic solvent surfactant extracts and a synthetic surfactant. Experiments were performed in the pulsating bubble surfactometer, with surfactant concentrations ranging between 0.1 and 2 mg.ml-1. Inhibition profiles towards fibrinogen, albumin and haemoglobin were obtained from calf lung surfactant extracts (CLSE), Alveofact, Curosurf and Survanta (all used in clinical, replacement studies in respiratory distress syndrome

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Horowitz, A. D., K. Kurak, B. Moussavian, et al. "Preferential uptake of small-aggregate fraction of pulmonary surfactant in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 273, no. 2 (1997): L468—L477. http://dx.doi.org/10.1152/ajplung.1997.273.2.l468.

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Abstract (sommario):

Homeostasis of pulmonary surfactant requires metabolic clearance of surfactant forms with decreased surface activity. Rabbit pulmonary surfactant was labeled in vivo with rhodamine-labeled dipalmitoylphosphatidylethanolamine (R-DPPE), isolated, and fractionated into large- and small-aggregate subfractions by differential centrifugation. Endocytosis of large (LA)- and small (SA)-aggregate surfactant by a mouse lung epithelial cell line (MLE-12) was evaluated in vitro by epifluorescence microscopy. More SA than LA surfactant was taken up by MLE-12 cells. Endocytosis of SA and LA surfactant was i

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Graham, Emma, Lynda McCaig, Gloria Shui-Kei Lau, et al. "E-cigarette aerosol exposure of pulmonary surfactant impairs its surface tension reducing function." PLOS ONE 17, no. 11 (2022): e0272475. http://dx.doi.org/10.1371/journal.pone.0272475.

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Abstract (sommario):

Introduction E-cigarette (EC) and vaping use continue to remain popular amongst teenage and young adult populations, despite several reports of vaping associated lung injury. One of the first compounds that EC aerosols comes into contact within the lungs during a deep inhalation is pulmonary surfactant. Impairment of surfactant’s critical surface tension reducing activity can contribute to lung dysfunction. Currently, information on how EC aerosols impacts pulmonary surfactant remains limited. We hypothesized that exposure to EC aerosol impairs the surface tension reducing ability of surfactan

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Fisher, James H., Vladimir Sheftelyevich, Ye-Shih Ho, et al. "Pulmonary-specific expression of SP-D corrects pulmonary lipid accumulation in SP-D gene-targeted mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 2 (2000): L365—L373. http://dx.doi.org/10.1152/ajplung.2000.278.2.l365.

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Abstract (sommario):

Targeted disruption of the surfactant protein (SP) D ( SP-D) gene caused a marked pulmonary lipoidosis characterized by increased alveolar lung phospholipids, demonstrating a previously unexpected role for SP-D in surfactant homeostasis. In the present study, we tested whether the local production of SP-D in the lung influenced surfactant content in SP-D-deficient [SP-D(−/−)] and SP-D wild-type [SP-D(+/+)] mice. Rat SP-D (rSP-D) was expressed under control of the human SP-C promoter, producing rSP-D, SP-D(+/+) transgenic mice. SP-D content in bronchoalveolar lavage fluid was increased 30- to 5

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Mokhber Dezfouli, Marzieh, Zohre Eftekhari, and Sirous Sadeghian Chaleshtori. "The Factors Effect on Natural Lung Surfactant Content for the Treatment of Respiratory Distress Syndrome." Iranian Journal of Veterinary Medicine 19, no. 1 (2025): 93–104. https://doi.org/10.32598/ijvm.19.1.1005467.

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Abstract (sommario):

Background: Exogenous surfactants from natural sources help restore normal lung function in premature cases. Pulmonary-surfactant dysfunction can lead to acute lung injury and is characterized by alveolar instability, floating, and collapse. These abnormalities occur in adult respiratory distress syndrome (ARDS) and neonatal respiratory distress syndrome (NRDS). Objectives: This study aimed to identify the best source of exogenous natural surfactant and its composition. Methods: Twenty-four healthy Holstein calves were selected in three age groups in both sexes to investigate the impact of sex

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