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Bronchoalveolar Lavage of Murine Lungs to Analyze Inflammatory Cell Infiltration
Published on: May 4, 2017
ADAM17 and related epithelial injury markers in bronchoalveolar lavage and blood distinguish COPD from controls
Carin E Lau1, Nicole M D van der Burg1, Jaro Ankerst1
1Department of Clinical Sciences Lund, Respiratory Medicine, Allergology and Palliative Medicine, Lund University, Lund, Sweden.
Background:
Chronic obstructive pulmonary disease (COPD) has many known dysregulated inflammatory proteins. A disintegrin and metalloproteinase 17 (ADAM17) is a protease that sheds several proteins involved in COPD pathogenesis. The aim was to investigate ADAM17, its phosphorylated form (pADAM17) and its substrates in bronchoalveolar lavage (BAL) and blood from COPD and control subjects.
Methods:
Groups were matched by sex, age, BMI and smoking status to compare between COPD, smoking and never smoking control subjects. The expression of ADAM17 and pADAM17 was assessed using immunofluorescence in BAL cells (n = 6-13). Concentrations of soluble ADAM17 and its substrates were quantified using ELISA or Luminex in BAL fluid (BALF, n = 11-14) and blood (n = 10-30).
Results:
COPD BAL samples had more ADAM17+ and pADAM17+ cells than controls and intracellular localisations were observed in epithelial cells of subjects with a smoking history. These elevations coincided with higher concentrations of several of the ADAM17 substrates in BALF from Smokers and COPD subjects, most prominently was the increased BALF HB-EGF found in COPD but not Smokers. Other changes in blood were also mostly related to epithelial injury and repair.
Conclusions:
Our findings highlight an overabundance of ADAM17 and pADAM17 in COPD airways that is accentuated beyond smoking-induced changes. This broad catalytic-complex analysis has both combined individual biomarkers and discovered more novel disease-specific biomarkers that may all relate to the overarching functionality of ADAM17 in COPD, warranting further investigation into the role this enzyme plays in COPD pathogenesis.
Insights
A disintegrin and metalloproteinase 17 (ADAM17) is elevated in chronic obstructive pulmonary disease (COPD) airways, exceeding smoking-related changes. This suggests ADAM17 plays a key role in COPD pathogenesis and may offer novel biomarkers.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Biochemistry
Background:
- Chronic obstructive pulmonary disease (COPD) is characterized by dysregulated inflammatory proteins.
- A disintegrin and metalloproteinase 17 (ADAM17), a protease, sheds proteins implicated in COPD pathogenesis.
Purpose of the Study:
- To investigate the expression and levels of ADAM17, its phosphorylated form (pADAM17), and its substrates.
- To compare these markers in bronchoalveolar lavage (BAL) and blood of COPD patients versus control subjects.
Main Methods:
- Matched groups (COPD, smokers, never-smokers) were analyzed for ADAM17 and pADAM17 expression via immunofluorescence in BAL cells.
- Soluble ADAM17 and substrate concentrations were measured using ELISA or Luminex in BAL fluid and blood.
Main Results:
- COPD BAL samples showed increased ADAM17+ and pADAM17+ cells compared to controls.
- Elevated ADAM17 substrates, notably HB-EGF, were found in BAL fluid of COPD patients.
- Blood changes were primarily linked to epithelial injury and repair processes.
Conclusions:
- ADAM17 and pADAM17 are significantly overabundant in COPD airways, surpassing smoking-induced effects.
- This study identified potential novel COPD-specific biomarkers related to ADAM17 activity.
- Further research is warranted to elucidate ADAM17's precise role in COPD pathogenesis.
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