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Published on: December 15, 2014
Association between the Reduced Expression of RECK and Neutrophilic Inflammation in Chronic Obstructive Pulmonary
Jiahui Wang1, Yi Su1, Hong Liu1
1Department of Pulmonary and Critical Care Medicine, Qingdao Municipal Hospital, University of Health and Rehabilitation Sciences, Qingdao, China.
Introduction:
Reversion-inducing cysteine-rich protein with Kazal motifs (RECK), a recently discovered inhibitor of matrix metalloproteinase (MMP). There is a large number of chronic obstructive pulmonary disease (COPD) patients worldwide; however, the role of RECK on COPD has not been studied. This study explored the expression of RECK in COPD patients and its effect on neutrophil function to provide a new scientific basis for the prevention and treatment of COPD.
Method:
Fifty patients with acute exacerbation of COPD and fifty healthy controls were enrolled in the study. RECK was detected in lung tissue, sputum, and plasma of subjects as well as in BEAS-2B cells stimulated with cigarette smoke extract (CSE) by immunohistochemistry, ELISA, and qRT-PCR. Meanwhile, lung function (FEV1%pred) and inflammatory cytokines (IL-6 and IL-8) were examined, and correlation analysis was performed with RECK expression. The effect of RECK on proliferation, apoptosis, migration, and inflammatory cytokines and its potential mechanism was further quantified by neutrophil stimulated with recombinant human RECK protein (rhRECK) combined with CSE using CCK8, flow cytometry, Transwell assay, qRT-PCR, ELISA, and Western analysis.
Results:
RECK was mainly expressed on airway epithelial cells in normal lung tissue and was significantly diminished in COPD patients. The levels of RECK in sputum and plasma were also significantly decreased in COPD patients. Pearson correlation analysis showed that RECK level in plasma was positively correlated with FEV1%pred (r = 0.458, p < 0.001) and negatively correlated with IL-6 and IL-8 (r = -0.386, -0.437; p = 0.006, 0.002) in COPD patients. The expression of RECK was decreased in BEAS-2B stimulated with CSE. The migration, inflammation, and MMP-9 expression of neutrophils were promoted by CSE, while inhibited by rhRECK.
Conclusion:
RECK is low expressed in COPD patients and negatively correlated with inflammation. It may inhibit the inflammation and migration of neutrophils by downregulating MMP-9.
Insights
Reversion-inducing cysteine-rich protein with Kazal motifs (RECK) is decreased in chronic obstructive pulmonary disease (COPD) patients and may inhibit neutrophil inflammation and migration by downregulating matrix metalloproteinase-9 (MMP-9). This finding offers a new basis for COPD prevention and treatment.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Immunology
Background:
- Reversion-inducing cysteine-rich protein with Kazal motifs (RECK) is a matrix metalloproteinase (MMP) inhibitor.
- Chronic obstructive pulmonary disease (COPD) affects millions globally, yet the role of RECK in COPD pathogenesis remains uninvestigated.
Purpose of the Study:
- To investigate RECK expression in COPD patients.
- To determine the effect of RECK on neutrophil function in COPD.
- To establish a scientific foundation for novel COPD therapeutic strategies.
Main Methods:
- RECK expression was analyzed in lung tissue, sputum, and plasma from COPD patients and healthy controls using immunohistochemistry, ELISA, and qRT-PCR.
- Lung function (FEV1%pred) and inflammatory cytokines (IL-6, IL-8) were assessed.
- Neutrophil function, including proliferation, apoptosis, migration, and inflammatory cytokine release, was evaluated in response to recombinant human RECK protein (rhRECK) and cigarette smoke extract (CSE).
Main Results:
- RECK expression was significantly diminished in airway epithelial cells, sputum, and plasma of COPD patients compared to controls.
- Plasma RECK levels positively correlated with lung function (FEV1%pred) and negatively correlated with IL-6 and IL-8 levels.
- CSE reduced RECK expression in BEAS-2B cells, while rhRECK inhibited CSE-induced neutrophil migration, inflammation, and MMP-9 expression.
Conclusions:
- RECK is downregulated in COPD patients and inversely associated with inflammation.
- RECK may exert anti-inflammatory and anti-migratory effects on neutrophils by suppressing MMP-9.
- Targeting RECK could represent a potential therapeutic approach for COPD management.
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