Euglena gracilis-derived β-glucan ameliorates particulate matter (PM2.5)-induced airway inflammation by modulating nuclear factor kappa B, mitogen-activated protein kinase, and nuclear factor erythroid 2-related factor 2 signaling pathways in A549 cells and BALB/c mice

This study aimed to investigate the effects of β-glucan derived from Euglena gracilis (EGB), an edible microalga, on particulate matter (PM2.5)-induced airway inflammation in A549 cells and BALB/c mice. EGB effectively suppressed the mRNA and protein levels of inflammatory cytokines (IL-6, IL-1β, TNF-α, IL-8) and mediators (iNOS, COX-2), while inhibiting the NF-κB and MAPK signaling pathways triggered by PM2.5 exposure and reducing nuclear NF-κB levels. Additionally, EGB decreased PM2.5-induced ROS production and increased the protein levels of NRF2 and HO-1, along with genes encoding antioxidant enzymes (catalase, GPx, SOD1), associated with elevated nuclear NRF2 levels. EGB reduced immune cell infiltration and inflammatory cytokine levels in BALF and serum, both of which increased by PM2.5 exposure. EGB also significantly increased alveolar numbers while decreasing the gene expression of MMP1/9/13. Furthermore, EGB suppressed PM2.5-induced bronchial thickening and collagen-1 deposition by downregulating TGF-β1 expression, and alleviated goblet cell hyperplasia and mucin production in lung tissues. These results suggest that EGB effectively reduces PM2.5-induced airway inflammation by suppressing NF-κB and MAPK signaling pathways, lowering pro-inflammatory cytokines, and activating the NRF2-HO-1 signaling pathway to enhance antioxidant enzyme expression. This study highlights the potential of EGB as an edible functional agent for controlling PM-related airway inflammation. [Display omitted] •EGB decreased inflammatory cytokine genes and boosted increased antioxidant enzymes genes.•EGB increased alveoli counts and decreased MMP expression in PM2.5-exposed mice.•EGB mitigated airway thickening and lowered TGF-β1 expression in PM2.5-exposed mice.•EGB alleviated PM2.5-induced mucin production and goblet hyperplasia in mice.•EGB suppressed NF-κB/MAPK signaling, while activating NRF2-HO-1 signaling pathway.