Ecklonia cava extract attenuates PM-exacerbated allergic asthma by modulating pulmonary macrophage polarization to suppress macrophage extracellular trap (MET) formation
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Published on: May 4, 2017
Hyo Jin Kim1, Manathunge Kumudu Sulakshani Thilakarathna2, Jiwon Yang2
1Department of Environmental Health, Harvard T.H. Chan School of Public Health, Harvard University, 665 Huntington, Boston, MA, 02115, USA; Department of Food Bioengineering, Jeju National University, 102 JeJudaehakno, Jeju, 63243, Republic of Korea.
Background:
Environmental particulate matter (PM) exacerbates allergic airway inflammation and promotes oxidative stress-driven immune dysregulation. Pulmonary macrophages are key mediators of these responses, and their polarization contributes to Th2/Th17-associated asthma pathology. Ecklonia cava ethanol extract (ECE), an edible brown alga, has anti-inflammatory potential.
Purpose:
This study investigated whether ECE attenuates PM-exacerbated allergic airway inflammation by regulating oxidative stress, pulmonary macrophage polarization, and macrophage extracellular trap (MET) formation.
Study Design:
MLE-12 lung epithelial cells and a PM-exacerbated allergic asthma mouse model were used to evaluate the protective effects of ECE.
Methods:
PM-induced oxidative stress and NF-κB activation were assessed in MLE-12 cells. In vivo, airway hyperresponsiveness, inflammatory cell infiltration, epithelial injury, mast cell activation, Th2/Th17 cytokine responses, oxidative stress in pulmonary macrophage, macrophage polarization, and MET formation were analyzed. A PAD4 inhibition model was used to evaluate CitH3-associated macrophage responses.
Results:
ECE suppressed PM-induced ROS production, MDA accumulation, p-IκBα expression, and NF-κB reporter activity in MLE-12 cells, with NAC supporting the involvement of oxidative stress. In PM-exacerbated allergic asthma mice, ECE reduced airway hyperresponsiveness, BALF inflammatory cells and protein levels, histopathological injury, mast cell degranulation, serum histamine, and Th2/Th17-associated cytokines. ECE also attenuated oxidative stress in pulmonary macrophage, reduced M1-associated markers, including CD80, Nos2, and iNOS, and suppressed M2-associated markers, including CD206, Arg1, and p-STAT6. Moreover, ECE decreased MET-related markers, including MPO, histone H3, MPO/CitH3, and F4/80/CitH3-positive macrophages. PAD4 inhibition further supported the involvement of CitH3-associated MET responses.
Conclusion:
ECE mitigates PM-exacerbated allergic airway inflammation by suppressing epithelial oxidative stress and NF-κB activation, in association with attenuated pulmonary macrophage polarization and MET formation. These findings suggest that ECE protects against PM-aggravated allergic asthma through coordinated regulation of oxidative stress and macrophage-mediated inflammatory responses.
Insights
Ecklonia cava extract (ECE) reduces particulate matter-induced allergic airway inflammation by decreasing oxidative stress and regulating pulmonary macrophage polarization and extracellular trap formation. This natural extract offers a potential therapeutic approach for managing PM-aggravated asthma.
Area of Science:
- Immunology
- Environmental Health
- Pharmacology
Background:
- Environmental particulate matter (PM) worsens allergic airway inflammation and immune imbalance through oxidative stress.
- Pulmonary macrophages are central to these responses, with their polarization driving Th2/Th17-associated asthma pathology.
- Ecklonia cava ethanol extract (ECE), derived from brown algae, exhibits potential anti-inflammatory properties.
Purpose of the Study:
- To determine if ECE can alleviate PM-induced allergic airway inflammation.
- To investigate ECE's effects on oxidative stress, pulmonary macrophage polarization, and macrophage extracellular trap (MET) formation in the context of PM exposure.
Main Methods:
- Utilized MLE-12 lung epithelial cells and a mouse model of PM-exacerbated allergic asthma to assess ECE's protective effects.
- Evaluated PM-induced oxidative stress, NF-κB activation, airway hyperresponsiveness, inflammatory cell infiltration, epithelial injury, mast cell activation, cytokine profiles, and macrophage polarization and MET formation.
- Employed PAD4 inhibition to further explore CitH3-associated macrophage responses.
Main Results:
- ECE suppressed PM-induced reactive oxygen species (ROS) production, oxidative damage markers, and NF-κB activation in lung cells.
- In vivo, ECE significantly reduced airway hyperresponsiveness, inflammation, tissue damage, mast cell degranulation, and Th2/Th17 cytokine levels.
- ECE attenuated oxidative stress in pulmonary macrophages, modulated M1/M2 polarization, and decreased the formation of macrophage extracellular traps (METs).
Conclusions:
- ECE effectively mitigates PM-exacerbated allergic airway inflammation.
- The protective effects are linked to the suppression of epithelial oxidative stress, NF-κB signaling, pulmonary macrophage polarization, and MET formation.
- ECE demonstrates potential as a therapeutic agent for PM-aggravated allergic asthma by coordinating anti-inflammatory and antioxidant pathways.
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