scholarly journals Surfactant Protein B Deficiency Induced High Surface Tension: Relationship between Alveolar Micromechanics, Alveolar Fluid Properties and Alveolar Epithelial Cell Injury

2019 ◽  
Vol 20 (17) ◽  
pp. 4243 ◽  
Author(s):  
Nina Rühl ◽  
Elena Lopez-Rodriguez ◽  
Karolin Albert ◽  
Bradford J Smith ◽  
Timothy E Weaver ◽  
...  
Keyword(s):  
Surface Tension ◽  
Lung Injury ◽  
High Surface ◽  
Surfactant Protein ◽  
Epithelial Injury ◽  
High Surface Tension ◽  
Alveolar Epithelial ◽  
Surfactant Protein B ◽  
Fluid Properties ◽  
Alveolar Epithelial Injury

High surface tension at the alveolar air-liquid interface is a typical feature of acute and chronic lung injury. However, the manner in which high surface tension contributes to lung injury is not well understood. This study investigated the relationship between abnormal alveolar micromechanics, alveolar epithelial injury, intra-alveolar fluid properties and remodeling in the conditional surfactant protein B (SP-B) knockout mouse model. Measurements of pulmonary mechanics, broncho-alveolar lavage fluid (BAL), and design-based stereology were performed as a function of time of SP-B deficiency. After one day of SP-B deficiency the volume of alveolar fluid V(alvfluid,par) as well as BAL protein and albumin levels were normal while the surface area of injured alveolar epithelium S(AEinjure,sep) was significantly increased. Alveoli and alveolar surface area could be recruited by increasing the air inflation pressure. Quasi-static pressure-volume loops were characterized by an increased hysteresis while the inspiratory capacity was reduced. After 3 days, an increase in V(alvfluid,par) as well as BAL protein and albumin levels were linked with a failure of both alveolar recruitment and airway pressure-dependent redistribution of alveolar fluid. Over time, V(alvfluid,par) increased exponentially with S(AEinjure,sep). In conclusion, high surface tension induces alveolar epithelial injury prior to edema formation. After passing a threshold, epithelial injury results in vascular leakage and exponential accumulation of alveolar fluid critically hampering alveolar recruitability.

Exoproduct secretions of Pseudomonas aeruginosa strains influence severity of alveolar epithelial injury

1994 ◽  
Vol 267 (5) ◽  
pp. L551-L556 ◽  
Author(s):  
I. Kudoh ◽  
J. P. Wiener-Kronish ◽  
S. Hashimoto ◽  
J. F. Pittet ◽  
D. Frank
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Lung Injury ◽  
Alveolar Epithelium ◽  
Infection Model ◽  
Epithelial Injury ◽  
Exoenzyme S ◽  
Alveolar Epithelial ◽  
Alveolar Epithelial Injury ◽  
Injury Control ◽  
Adp Ribosyltransferase

To determine whether exoenzyme S plays a role in alveolar epithelial injury, two parental strains of Pseudomonas aeruginosa, PAK and PA103, were tested that produced large quantities of exoenzyme S. Strains PAK and PA103 differ in the form of exoenzyme S they produce. Strain PAK produces a 53-kDa protein that does not possess ADP-ribosyltransferase activity and large quantities of a 49-kDa protein that expresses ADP-ribosyltransferase activity. Strain PA103 produces the 53-kDa protein and low amounts of exoenzyme S activity. A quantitative experimental protocol was used to measure the protein permeability of the alveolar epithelium and the dissemination of the bacteria to the pleural space and circulation. The results indicate that instillation of PAK and PA103 resulted in significant lung injury. Control experiments utilizing isogenic, exoenzyme S-deficient, regulatory mutants in the infection model reduced the lung injury and the dissemination of instilled bacteria. Taken together these results suggest that alveolar epithelial injury correlated with the production of the 53-kDa form of exoenzyme S or other coordinately regulated factors.

The influence of genetic variation in surfactant protein B on severe lung injury in African American children*

2011 ◽  
Vol 39 (5) ◽  
pp. 1138-1144 ◽  
Author(s):  
Mary K. Dahmer ◽  
Peggy OʼCain ◽  
Pallavi P. Patwari ◽  
Pippa Simpson ◽  
Shun-Hwa Li ◽  
...  
Keyword(s):  
Genetic Variation ◽  
African American ◽  
Lung Injury ◽  
Surfactant Protein ◽  
African American Children ◽  
Surfactant Protein B ◽  
American Children ◽  
Severe Lung ◽  
Protein B

scholarly journals 355 ABNORMALLY HIGH SURFACE TENSION OF LUNG SURFACTANT IN 2 INFANTS WITH SEVERE APPARENT LIFE-THREATENING EVENTS (ALTE)

1994 ◽  
Vol 36 (1) ◽  
pp. 62A-62A
Author(s):  
Christian F Poets ◽  
Ilona Martin ◽  
Christa Acevedo ◽  
Kristin Neuber ◽  
Anne Rudolph ◽  
...  
Keyword(s):  
Surface Tension ◽  
High Surface ◽  
Lung Surfactant ◽  
High Surface Tension ◽  
Life Threatening

Distinct effects of oxygen on surfactant protein B expression in bronchiolar and alveolar epithelium

1992 ◽  
Vol 262 (1) ◽  
pp. L32-L39 ◽  
Author(s):  
K. A. Wikenheiser ◽  
S. E. Wert ◽  
J. R. Wispe ◽  
M. Stahlman ◽  
M. D'Amore-Bruno ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Alveolar Epithelium ◽  
Surfactant Protein ◽  
Alveolar Epithelial Cells ◽  
Cell Protein ◽  
Altered Expression ◽  
Alveolar Epithelial ◽  
Surfactant Protein B ◽  
Bronchiolar Epithelium ◽  
Protein B

Hyperoxia causes severe lung injury in association with altered expression of surfactant proteins and lipids. To test whether oxygen induces surfactant protein B (SP-B) expression in specific respiratory epithelial cells, adult B6C3F1 and FVB/N mice were exposed to room air or 95% oxygen for 1–5 days. Northern blot analysis demonstrated an 8- to 10-fold increase in SP-B mRNA after 3 days that was maintained thereafter. In situ hybridization localized SP-B mRNA to bronchial, bronchiolar, and alveolar epithelial cells. Hyperoxia was associated with increased SP-B mRNA, noted primarily in the bronchiolar epithelium and decreased SP-B mRNA in the alveolar epithelium. After 5 days, central regions of lung parenchyma were nearly devoid of SP-B mRNA, while SP-B mRNA was maintained in alveolar cell populations close to vascular structures. To determine whether increased bronchiolar expression of SP-B mRNA during hyperoxia was a specific response, the abundance of CC10 mRNA (a Clara cell protein) was assessed. CC10 mRNA was detected in tracheal, bronchial, and bronchiolar, but not alveolar epithelium and was decreased upon exposure to hyperoxia. Immunocytochemistry demonstrated that SP-B proprotein was detected in bronchial, bronchiolar, and alveolar epithelial cells with staining increased in the bronchial and bronchiolar epithelium upon exposure to hyperoxia. SP-B gene expression in the respiratory epithelium is regulated at a pretranslational level and occurs in a cell specific manner during hyperoxic injury in the mouse.

The late asthmatic response is linked with increased surface tension and reduced surfactant protein B in mice

2002 ◽  
Vol 283 (4) ◽  
pp. L755-L765 ◽  
Author(s):  
Angela Haczku ◽  
Elena N. Atochina ◽  
Yaniv Tomer ◽  
Yang Cao ◽  
Colleen Campbell ◽  
...  
Keyword(s):  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Late Phase ◽  
Surfactant Protein ◽  
Intratracheal Administration ◽  
Asthmatic Response ◽  
Surfactant Protein B ◽  
Airway Response ◽  
Allergen Provocation ◽  
Surfactant Dysfunction

Pulmonary surfactant dysfunction may significantly contribute to small airway obstruction during the asthmatic response, but neither its exact role nor its regulation is clear. Surfactant function and composition was studied in an Aspergillus fumigatus ( Af)-induced late-phase allergic airway response in sensitized BALB/c mice. The peak of Af-induced airway hyperresponsiveness in sensitized and challenged mice 24 h after allergen provocation coincided with a significant fall in surface activity of the pulmonary surfactant. The underlying changes included time-dependent elaboration of eotaxin and IL-5 followed by eosinophil influx into the airways. The height of airway inflammation and hyperresponsiveness was preceded by release of IL-4 and marked reductions in surfactant protein (SP)-B, a hydrophobic surfactant protein responsible for maintaining low surface tension of the lining fluid of distal air spaces. Furthermore, intratracheal administration of IL-4 significantly inhibited SP-B, indicating a regulatory role of this cytokine in the surfactant biophysical changes. Thus surfactant dysfunction induced by an IL-4-driven SP-B deficiency after allergen provocation may be an important part of the late asthmatic airway response.

Rheological Properties of Liquid Metals and Semisolid Materials at Low Solid Fraction

2016 ◽  
Vol 256 ◽  
pp. 133-138 ◽  
Author(s):  
Marialaura Tocci ◽  
Christoph Zang ◽  
Ines Cadòrniga Zueco ◽  
Annalisa Pola ◽  
Michael Modigell
Keyword(s):  
Surface Tension ◽  
Rheological Properties ◽  
Liquid Metals ◽  
High Surface ◽  
Measuring System ◽  
High Surface Tension ◽  
Viscous Forces ◽  
Low Viscosity ◽  
Semi Solid ◽  
Low Shear

Rheological properties of liquid metals are difficult to investigate experimentally because of the extreme border conditions to consider. One difficulty is related to the low viscosity of liquid metals. Surface tension effects can cause forces that can be considerably higher than the viscous forces in the liquid metals. Evaluating the experimental data without considering these effects leads to an apparent shear thinning behavior of the material. In the present study, experiments were performed by means of a Searle rheometer changing the dimension of the measuring system with metals of high surface tension, as mercury and tin. It became evident that surface tension plays a significant role in the effects that falsify measurements at low shear rate. Conclusions can be drawn to what extent measurements of semi-solid metals are affected.

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