Alveolar Epithelial Injury Causing Respiratory Distress in Dogs

CHEST Journal ◽  
1979 ◽  
Vol 75 (6) ◽  
pp. 705-711 ◽  
Author(s):  
C. Redington Barrett ◽  
A.L. Loomis Bell ◽  
Stephen F. Ryan
Keyword(s):  
Respiratory Distress ◽  
Epithelial Injury ◽  
Alveolar Epithelial ◽  
Alveolar Epithelial Injury

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.

Detection of alveolar epithelial injury by Tc-99m DTPA radioaerosol inhalation lung scan in rheumatoid arthritis patients

2005 ◽  
Vol 19 (6) ◽  
pp. 455-460 ◽  
Author(s):  
Berna Okudan ◽  
Mehmet Şahİn ◽  
Feride Meltem Özbek ◽  
Ali Ümit Keskİn ◽  
Erkan Cüre
Keyword(s):  
Rheumatoid Arthritis ◽  
Epithelial Injury ◽  
Alveolar Epithelial ◽  
Lung Scan ◽  
Alveolar Epithelial Injury

scholarly journals Differential alveolar epithelial injury and protein expression in pneumococcal pneumonia

2012 ◽  
Vol 38 (5) ◽  
pp. 266-276 ◽  
Author(s):  
Christine Tyrrell ◽  
Stuart R. McKechnie ◽  
Michael F. Beers ◽  
Tim J. Mitchell ◽  
Mary C. McElroy
Keyword(s):  
Protein Expression ◽  
Pneumococcal Pneumonia ◽  
Epithelial Injury ◽  
Alveolar Epithelial ◽  
Alveolar Epithelial Injury

scholarly journals Analyses of alveolar epithelial injury via lipid-related stress in mammalian target of rapamycin inhibitor-induced lung disease

2019 ◽  
Vol 99 (6) ◽  
pp. 853-865
Author(s):  
Nariaki Kokuho ◽  
Yasuhiro Terasaki ◽  
Shinobu Kunugi ◽  
Yoshinobu Saito ◽  
Hirokazu Urushiyama ◽  
...  
Keyword(s):  
Lung Disease ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Epithelial Injury ◽  
Alveolar Epithelial ◽  
Alveolar Epithelial Injury ◽  
Related Stress

scholarly journals Idiopathic Pulmonary Fibrosis: Treatment and Prognosis

2015 ◽  
Vol 9s1 ◽  
pp. CCRPM.S23321 ◽  
Author(s):  
Hajime Fujimoto ◽  
Tetsu Kobayashi ◽  
Arata Azuma
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Treatment Options ◽  
Additional Treatment ◽  
Treatment Modalities ◽  
Epithelial Injury ◽  
Alveolar Epithelial ◽  
Alveolar Epithelial Injury ◽  
Long Term Oxygen Therapy

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease with a prognosis that can be worse than for many cancers. The initial stages of the condition were thought to mainly involve chronic inflammation; therefore, corticosteroids and other drugs that have anti-inflammatory and immunosuppressive actions were used. However, recently, agents targeting persistent fibrosis resulting from aberrant repair of alveolar epithelial injury have been in the spotlight. There has also been an increase in the number of available antifibrotic treatment options, starting with pirfenidone and nintedanib. These drugs prevent deterioration but do not improve IPF. Therefore, nonpharmacologic approaches such as long-term oxygen therapy, pulmonary rehabilitation, and lung transplantation must be considered as additional treatment modalities.

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.

scholarly journals Distinct Time Courses and Pathogenic Contributions of Alveolar Epithelial and Endothelial Injury in Acute Respiratory Distress Syndrome With COVID-19: Evidence From Circulating Biomarkers

2021 ◽  
Author(s):  
Kentaro Tojo ◽  
Natsuhiro Yamamoto ◽  
Takahiro Mihara ◽  
Miyo Abe ◽  
Takahisa Goto
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Tissue Injury ◽  
Endothelial Injury ◽  
Epithelial Injury ◽  
Alveolar Epithelial ◽  
Srage Level ◽  
Alveolar Tissue

Abstract Background: In severe cases of coronavirus disease (COVID-19), acute respiratory distress syndrome (ARDS) with alveolar tissue injury occurs. However, the time course and specific contributions of alveolar epithelial and endothelial injury to the pathogenesis of COVID-19 ARDS remain unclear.Methods: We evaluated the levels of a circulating alveolar epithelial injury marker (soluble receptor for advanced glycation end-products: sRAGE) and an endothelial injury marker (angiopoietin-2: ANG-2), along with an alveolar permeability indicator (surfactant protein D: SP-D) in 107 serum samples from nine patients with ARDS and eight without ARDS, all with COVID-19, admitted to Yokohama City University Hospital from January to July 2020. We compared the initial levels of these markers between ARDS and non-ARDS patients, and analysed the temporal changes of these markers in ARDS patients. Results: All the initial levels of sRAGE (median: 2680 pg/mL, IQR:1522–5076 vs. median 701 pg/mL, IQR:344–1148.0, p=0.0152), ANG-2 (median: 699 pg/mL, IQR: 410-2501 vs. median: 231 pg/mL, IQR: 64-584, p=0.0464), and SP-D (median: 17542 pg/mL, IQR: 7423-22979 vs. 1771 pg/mL, IQR: 458-204, p=0.0274) were significantly higher in the ARDS patients than in the non-ARDS patients. The peak sRAGE level in the ARDS patients was observed at the very early phase of disease progression (median: day 1, IQR: day 1–3.5). However, the peaks of ANG-2 (median: day 4, IQR: day 2.5–6) and SPD (median: day 5, IQR: day 3–7.5) were observed at a later phase. Moreover, the ANG-2 level was significantly correlated with the arterial oxygenation (p=0.030) and the SPD level (p=0.002), but the sRAGE level was not. Conclusion: Evaluation of circulating markers confirms that COVID-19 ARDS is characterised by severe alveolar tissue injury. Our data indicate that the endothelial injury, which continues for a longer period than the epithelial injury, seems to be the main contributor to alveolar barrier disruption. Targeting the endothelial injury may, thus, be a promising approach to overcome ARDS with COVID-19.

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