Related Experiment Video
Updated: Jun 14, 2026
Detection of Functional Matrix Metalloproteinases by Zymography
Published on: November 8, 2010
Serum metalloproteinase leukolysin (MMP-25/MT-6): a potential metabolic marker for atopy-associated inflammation
M N Blumenthal1, W Zhong, M Miller
1Department of Medicine, The Asthma and Allergy Center, University of Minnesota Medical School, Minneapolis, MN 55455, USA. blume001@umn.edu
Background:
Leukolysin is a novel matrix metalloproteinase (MMP-25/MT-6) released mainly by granulocytic cells, primarily neutrophils, which are implicated in chronic airways inflammation.
Objective:
To determine if leukolysin might be a serum marker for atopic asthma or chronic obstructive pulmonary disease (COPD).
Methods:
Three study populations were evaluated: (1) nuclear families with medical history of atopic asthma (N=337), (2) married-in individuals from an independent study of asthma genetics (N=122) and (3) randomly selected males with diagnosis of COPD (N=100). Each person was screened for asthma or COPD symptoms, respiratory function by standardized spirometry and serum total IgE and leukolysin and anti-IL1 levels by immunoassay. Study groups (1 and 2) were also screened by skin prick test using a battery of 14 common aeroallergens. Heritability estimates for leukolysin and total IgE were made by variance components analysis.
Results:
For those without asthma or who had asthma defined as having symptoms, a physician's diagnosis and bronchial hyper-reactivity as demonstrated by reversibility in response to albuteral and/or bronchial reactivity as measured by a methacholine challenge, serum leukolysin levels were found to be higher for those with any positive skin test result. This paralleled trends for serum total IgE. In the nuclear families and COPD patients, serum leukolysin levels were significantly elevated for those who also had elevated total IgE levels (log[IgE]>2.0) compared with those with lower IgE (log[IgE]<2.0). Serum IL-1 levels correlated with the leukolycin levels. In contrast to IgE, leukolysin showed no apparent inherited component.
Conclusion:
Among individuals with history of chronic airways inflammation (asthma and COPD) serum leukolysin may be a metabolic marker associated with chronic atopy-associated respiratory inflammation. Common factors may stimulate increased production or release of both leukolysin from myeloid cells and IgE from lymphoid cells.
Insights
Leukolysin, a protein released by neutrophils, may serve as a serum marker for atopic asthma and chronic obstructive pulmonary disease (COPD). Elevated leukolysin levels correlate with atopy-associated respiratory inflammation, but it is not an inherited marker.
Area of Science:
- Immunology
- Respiratory Medicine
- Biochemistry
Background:
- Leukolysin (MMP-25/MT-6) is released by granulocytic cells, particularly neutrophils.
- Neutrophils are implicated in the pathogenesis of chronic airways inflammation.
Purpose of the Study:
- To investigate leukolysin as a potential serum biomarker for atopic asthma and COPD.
- To explore the relationship between leukolysin, IgE, and IL-1 levels in respiratory diseases.
Main Methods:
- Evaluated three populations: families with asthma, asthma genetics study participants, and COPD patients.
- Assessed respiratory symptoms, pulmonary function, serum total IgE, leukolysin, and anti-IL-1 levels via immunoassay.
- Utilized skin prick tests and variance components analysis for heritability estimates.
Main Results:
- Higher serum leukolysin levels were observed in individuals with positive skin tests, mirroring total IgE trends.
- Leukolysin levels were significantly elevated in asthma and COPD patients with high total IgE.
- Serum IL-1 levels correlated with leukolysin levels; leukolysin showed no inherited component.
Conclusions:
- Serum leukolysin may indicate chronic atopy-associated respiratory inflammation in asthma and COPD.
- Common factors might drive the production of both leukolysin and IgE.
- Leukolysin's role as a metabolic marker in chronic respiratory conditions warrants further investigation.
