Redox biology · 2025
Particulate matter exposure induces pulmonary TH2 responses and oxidative stress-mediated NRF2 activation in mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Jo Yuna, Kim Bo-Young, Lee So Min, Park Jisu, Kim Wooseok, Shim Ju A, Park Jun Hong, Park Jong-Eun, Shin Yong-Il, Ryu Ji Hyeon, Hong Changwan
Аннотация
INTRODUCTION: Particulate matter (PM) is a harmful air pollutant associated with respiratory and cardiovascular diseases, but its effects on adaptive immunity are poorly understood.
OBJECTIVES: This study investigates the role of NRF2 in T cells in mediating immune and pulmonary responses to long-term PM exposure, highlighting its impact on inhalation toxicity.
METHODS: To establish a mouse model of lung injury induced by PM exposure, C57BL/6 mice were intranasally administered 20 μg/kg PM10 or PM2.5 daily for 16 weeks. Lung injury parameters were analyzed in bronchoalveolar lavage fluid (BALF), plasma, and lung tissue. Changes in the proportion of immune cells in the lymph nodes and spleen were analyzed.
RESULTS: Mice exposed to PM for 16 weeks showed severe lung damage, such as inflammatory cell infiltration, thickened alveolar walls, and increased oxidative stress and apoptosis. PM exposure also increased collagen and fibronectin levels, indicating tissue remodeling. Immune cell analysis revealed reduced B cell expansion, increased IL-4-producing CD4+ T cells, and decreased IFN-γ- and TNF-α-producing CD4+ T cells, accompanied by higher TH2 cytokines and plasma IgE and IgG1 levels. PM activated the NRF2 pathway, skewing immune responses toward TH2 differentiation, which worsened lung inflammation.
CONCLUSIONS: These findings highlight how PM exposure disrupts immune balance and exacerbates conditions like asthma and chronic obstructive pulmonary disease by promoting TH2-driven inflammation through NRF2 activation.
OBJECTIVES: This study investigates the role of NRF2 in T cells in mediating immune and pulmonary responses to long-term PM exposure, highlighting its impact on inhalation toxicity.
METHODS: To establish a mouse model of lung injury induced by PM exposure, C57BL/6 mice were intranasally administered 20 μg/kg PM10 or PM2.5 daily for 16 weeks. Lung injury parameters were analyzed in bronchoalveolar lavage fluid (BALF), plasma, and lung tissue. Changes in the proportion of immune cells in the lymph nodes and spleen were analyzed.
RESULTS: Mice exposed to PM for 16 weeks showed severe lung damage, such as inflammatory cell infiltration, thickened alveolar walls, and increased oxidative stress and apoptosis. PM exposure also increased collagen and fibronectin levels, indicating tissue remodeling. Immune cell analysis revealed reduced B cell expansion, increased IL-4-producing CD4+ T cells, and decreased IFN-γ- and TNF-α-producing CD4+ T cells, accompanied by higher TH2 cytokines and plasma IgE and IgG1 levels. PM activated the NRF2 pathway, skewing immune responses toward TH2 differentiation, which worsened lung inflammation.
CONCLUSIONS: These findings highlight how PM exposure disrupts immune balance and exacerbates conditions like asthma and chronic obstructive pulmonary disease by promoting TH2-driven inflammation through NRF2 activation.