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조회51

Harvard University, 제주대학교

Phytomedicine, 11 July 2026, 159 S0944-7113(26)00741-5 | https://doi.org/10.1016/j.phymed.2026.158510 Ecklonia cava extract attenuates PM-exacerbated allergic asthma by modulating pulmonary macrophage polarization to suppress macrophage extracellular trap (MET) formation

Hyo Jin Kim ^a,b, Manathunge Kumudu Sulakshani Thilakarathna ^c, Jiwon Yang ^c, Gamaralalage Prabhavi Dayaddra ^c, Mi-Ok Ko ^c, Kalahe Hewage Iresha Nadeeka Madushani Herath ^d, Minhyeok Kang ^c, You-Jin Jeon ^e, Seung Mi Ko ^f, Soo Youn Choi ^f, Chan Young Kim^f, Youngheun Jee ^c,g

^aDepartment of Environmental Health, Harvard T.H. Chan School of Public Health, Harvard University, 665 Huntington, Boston, MA, 02115, USA
^bDepartment of Food Bioengineering, Jeju National University, 102 JeJudaehakno, Jeju, 63243, Republic of Korea
^cInterdisciplinary Graduate Program in Advanced Convergence Technology & Science, Jeju National University, Jeju, 63243, Republic of Korea
^dDepartment of Biosystems Engineering, Faculty of Agriculture and Plantation Management, Wayamba University, Gonawila, Sri Lanka
^eDepartment of Marine Life science, School of Marine Biomedical Sciencs, Jeju National University, Jeju, 690-756, Republic of Korea
^fDepartment of Biology, College of Natural Sciences Jeju National University, Jeju, 63243, Republic of Korea
^gDepartment of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, 102 Jejudaehakno, Jeju, 63243, Republic of Korea

Corresponding author : Youngheun Jee

Abstract

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.

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