Mechanisms underlying Th2-dominant pneumonia caused by plastic pollution derivatives (PPD): A molecular toxicology investigation that encompasses gut microbiomics and lung metabolomics

• Published in: Journal of hazardous materials 2024-12, Vol.480, p.136326, Article 136326
• Main Authors: Lu, Surui, Feng, Qing, Chen, Mingqing, Zeng, Xin, Wei, Huaqin, Chen, Qizi, Guo, Hai, Su, Liqin, Yan, Biao, Wu, Yang, Yang, Xu, Ma, Ping
• Format: Article
• Language: English
• Subjects: Animals; Deferoxamine - pharmacology; Dibutyl Phthalate - toxicity; Ferroptosis - drug effects; Gastrointestinal Microbiome - drug effects; Gut microbiome; Lung - drug effects; Lung - metabolism; Lung - pathology; Male; Metabolomics; Mice; Microplastics - toxicity; Oxidative Stress - drug effects; Plastic pollution derivatives (PPD); Pneumonia - chemically induced; Pneumonia - metabolism; Polystyrenes - toxicity; Reactive Oxygen Species - metabolism; Short chain fatty acid (SCFA); Th2 Cells - drug effects; Th2 Cells - immunology; Th2-predominant pneumonia
• ISSN: 0304-3894; 1873-3336; 1873-3336
• DOI: 10.1016/j.jhazmat.2024.136326

An investigation was conducted by researchers on how dibutyl phthalate (DBP) and polystyrene microplastics (PS-MP) influence the development of pneumonia using a mouse model. For a duration of five weeks, the mice were subjected to exposure of DBP (30 mg/kg/day) and PS-MP (0.1 mg/day). The findings indicated notable pathological alterations in airway tissues, increased oxidative stress levels, and intensified inflammation, thereby establishing a connection between plastic pollution and pneumonia. Further examination indicated the involvement of ferroptosis and oxidative stress in the progression of the disease. Administration of deferoxamine (DFO) (100 mg/kg) resulted in symptom relief and reduced pathological alterations, as validated by metabolomic investigations. Increased levels of reactive oxygen species (ROS) triggered a Th2-mediated eosinophilic inflammatory response, marked by elevated IL-4 and reduced IFN-γ via the NFκB pathway. Moreover, analyses of the gut microbiome and metabolomics demonstrated that PPD modifies microbial populations and pulmonary metabolism, linking its effects on pneumonia through the gut-lung axis. This research highlights the health hazards associated with plastic pollution and proposes a framework for tackling these issues. [Display omitted] •A new concept of plastic derivatives was proposed, and a model for PPD was created in this study.•PPD-induced pneumonia involved in both chemical and Th2-predominant pneumonia.•Lung cell ferroptosis and NFκB pathway mediated the ROS induced Th2-predominant pneumonia.•PPD can induce the occurrence of pneumonia by altering the gut microbiota composition.