We have located links that may give you full text access.
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Pallid mice with genetic emphysema. Neutrophil elastase burden and elastin loss occur without alteration in the bronchoalveolar lavage cell population.
BACKGROUND: According to a current hypothesis, pulmonary emphysema results from damage to the elastic fiber network caused by an imbalance within the lower respiratory tract between elastase(s) and protease inhibitors. This hypothesis is based largely on studies of persons with genetic deficiency of serum alpha 1-proteinase inhibitor. We recently reported a spontaneously occurring emphysema in the pallid mouse with an inherited deficiency of serum alpha 1-proteinase inhibitor. This animal reproduces important features of the human condition. We describe here the changes in alveolar elastolytic burden and in the bronchoalveolar lavage (BAL) cell population, which precede and accompany the development of emphysema in pallid mice.
EXPERIMENTAL DESIGN: A possible correlation between the levels of lung elastase burden and the loss of lung elastin content was investigated in the period of development of emphysema in pallid mice. Changes in alveolar cells were investigated for specimens from BAL fluids and lung tissue by cytologic, histologic, and immunogold-electron microscopic methods.
RESULTS: An immunogold-positive reaction for elastase was observed on elastin within the alveolar walls of pallid mice from 2 months onward. The average of gold particle density progressively increased with age, reaching high values at 12 and 16 months of age, the age at which parenchymal destruction was previously reported to occur. Lung elastin content had normal values at 2, 4, and 8 months of age. However, it was significantly lower at 12 and 16 months of age. The immunogold values of elastase burden correlated inversely with the decrease in lung elastin content. Total and differential cell counts from BAL fluids of pallid mice did not differ significantly at any time in life and were similar to age-matched controls. However, in pallid mice from 8 months of life onward, pulmonary macrophages contained characteristic intracytoplasmic crystalloid inclusions, which were electrondense and bounded by a single membrane. Using electron microscopy and an immunogold-labeling technique with anti-mouse I-III collagen IgG, these inclusions were identified as collagen-derived products.
CONCLUSIONS: The data reported in this paper suggest that emphysematous lesions in pallid mice are associated with a progressive increase of elastase in alveolar intestitium and with loss of lung elastin. Surprisingly, the number of neutrophils in BAL fluids does not increase with the increase of lung elastolytic burden. However, intracytoplasmic crystalloid inclusions related to collagen degradation were observed in pulmonary macrophages of pallid mice at the time of septal disruption. The presence of similar structures in alveolar macrophages from mice or other animal species may be indicative of connective tissue breakdown or remodeling of tissue collagen.
EXPERIMENTAL DESIGN: A possible correlation between the levels of lung elastase burden and the loss of lung elastin content was investigated in the period of development of emphysema in pallid mice. Changes in alveolar cells were investigated for specimens from BAL fluids and lung tissue by cytologic, histologic, and immunogold-electron microscopic methods.
RESULTS: An immunogold-positive reaction for elastase was observed on elastin within the alveolar walls of pallid mice from 2 months onward. The average of gold particle density progressively increased with age, reaching high values at 12 and 16 months of age, the age at which parenchymal destruction was previously reported to occur. Lung elastin content had normal values at 2, 4, and 8 months of age. However, it was significantly lower at 12 and 16 months of age. The immunogold values of elastase burden correlated inversely with the decrease in lung elastin content. Total and differential cell counts from BAL fluids of pallid mice did not differ significantly at any time in life and were similar to age-matched controls. However, in pallid mice from 8 months of life onward, pulmonary macrophages contained characteristic intracytoplasmic crystalloid inclusions, which were electrondense and bounded by a single membrane. Using electron microscopy and an immunogold-labeling technique with anti-mouse I-III collagen IgG, these inclusions were identified as collagen-derived products.
CONCLUSIONS: The data reported in this paper suggest that emphysematous lesions in pallid mice are associated with a progressive increase of elastase in alveolar intestitium and with loss of lung elastin. Surprisingly, the number of neutrophils in BAL fluids does not increase with the increase of lung elastolytic burden. However, intracytoplasmic crystalloid inclusions related to collagen degradation were observed in pulmonary macrophages of pallid mice at the time of septal disruption. The presence of similar structures in alveolar macrophages from mice or other animal species may be indicative of connective tissue breakdown or remodeling of tissue collagen.
Full text links
Trending Papers
A Personalized Approach to the Management of Congestion in Acute Heart Failure.Heart International 2023
Potential Mechanisms of the Protective Effects of the Cardiometabolic Drugs Type-2 Sodium-Glucose Transporter Inhibitors and Glucagon-like Peptide-1 Receptor Agonists in Heart Failure.International Journal of Molecular Sciences 2024 Februrary 21
2024 ACC Expert Consensus Decision Pathway for Treatment of Heart Failure With Reduced Ejection Fraction: A Report of the American College of Cardiology Solution Set Oversight Committee.Journal of the American College of Cardiology 2024 March 3
The Effect of Albumin Administration in Critically Ill Patients: A Retrospective Single-Center Analysis.Critical Care Medicine 2024 Februrary 8
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app