Abstract Title:

Fine Particulate Matter and Sulfur Dioxide Coexposures Induce Rat Lung Pathological Injury and Inflammatory Responses Via TLR4/p38/NF-κB Pathway.

Abstract Source:

Int J Toxicol. 2017 Mar/Apr;36(2):165-173. Epub 2016 Dec 29. PMID: 28033732

Abstract Author(s):

Ruijin Li, Lifang Zhao, Jinlong Tong, Yuchao Yan, Chong Xu

Article Affiliation:

Ruijin Li


Fine particulate matter (PM) and sulfur dioxide (SO) are 2 common air pollutants, but their toxicological effects of coexposure are still not fully clear. In this study, SOexposure (5.6 mg/m) couldn't cause obvious inflammatory responses in rat lungs. The PMexposure (1.5 mg/kg body weight) increased inflammatory cell counts in bronchoalveolar lavage fluid (BALF) and some inflammation damage. Importantly, SOand PM(1.5, 6.0, and 24.0 mg/kg) coexposure induced pathological and ultrastructural damage and raised inflammatory cells in BALF compared with the control. Also, they significantly elevated the levels of pro-inflammatory cytokines, adhesion molecule, and nitric oxide (NO) and promoted the gene expression of nuclear factor kappa B (NF-κB), phosphorylated p38 (p-p38), and Toll-like receptor 4 (TLR4) in rat lungs treated with higher dose of PM(6.0 and 24.0 mg/kg) plus SOrelative to the control or SOgroup, along with the decreased inhibitor of NF-κBα and increased inhibitor of NF-κB kinase β expressions. The changes in the inflammatory markers in the presence of PMplus SOwere not significant compared with the PMgroup. The results indicated that inflammatory injury and pathological and ultrastructural damage in rat lungs exposed to PMplus SOwere involved in TLR4/p38/NF-κB pathway activation accompanied by oversecretion of pro-inflammatory cytokine, adhesion molecule, and NO. It provides more useful evidence to understand the possible toxicological mechanism that PMand SOcopollution exacerbate lung disease.

Study Type : Animal Study

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