Predictive and Prognostic Biomarkers of Respiratory Diseases due to Particulate Matter Exposure

Kim, Hyo Jeong; Choi, Min Gi; Park, Moo Kyun; Seo, Young Rok

doi:10.15430/jcp.2017.22.1.6

Cited by 76 publications

(36 citation statements)

References 96 publications

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“…A growing body of epidemiological evidence suggests that exposure to PM is closely correlated with the mortality and morbidity of respiratory diseases (Kim et al 2017). However, the pathophysiological processes triggered by PM exposure are complex, involving mucus hyperproduction, bronchial epithelial injury, and impaired airway antibacterial defense leading to loss of epithelial integrity (Aloui et al 2016;Chen et al 2018;Xu et al 2018a;.…”

Section: Discussionmentioning

confidence: 99%

Evidence for the critical role of the PI3K signaling pathway in particulate matter-induced dysregulation of the inflammatory mediators COX-2/PGE2 and the associated epithelial barrier protein Filaggrin in the bronchial epithelium

et al. 2019

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Particulate matter (PM) is an environmental pollutant closely associated with human airway inflammation. However, the molecular mechanisms of PMrelated airway inflammation remains to be fully elucidated. It is known that COX-2/PGE 2 play key roles in the pathogenesis of airway inflammation. Filaggrin is a transmembrane protein contributing to tight junction barrier function. As such, Filaggrin prevents leakage of transported solutes and is therefore necessary for the maintenance of epithelial integrity. The objective of the present study was to investigate the regulatory mechanisms of COX-2/PGE 2 and Filaggrin upon PM exposure both in vivo and in vitro. C57BL/6 mice received intratracheal instillation of PM for two consecutive days. In parallel, human bronchial epithelial cells (HBECs) were exposed to PM for 24 h. PM exposure resulted in airway inflammation together with upregulation of COX-2/PGE 2 and downregulation of Filaggrin in mouse lungs. Corresponding dysregulation of COX-2/ PGE 2 and Filaggrin was also observed in HBECs subjected to PM. PM exposure led to the phosphorylation of ERK, JNK, and PI3K signaling pathways in a time

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Section: Discussionmentioning

confidence: 99%

Evidence for the critical role of the PI3K signaling pathway in particulate matter-induced dysregulation of the inflammatory mediators COX-2/PGE2 and the associated epithelial barrier protein Filaggrin in the bronchial epithelium

et al. 2019

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“…Finally, it was interesting to note the significant modulation of genes involved in post-translational and epigenetic modifications. The identification of the resulting biological effects of such modifications was beyond the scope of the present study, but it is clear that they could be of major importance given their involvement in (lung) disease progression 25 . Overall, our findings highlight and illustrate the importance of the necessity to go beyond the “classical” pathways that are traditionally investigated in the nanotoxicological context.…”

Section: Discussionmentioning

confidence: 98%

Substantial modification of the gene expression profile following exposure of macrophages to welding-related nanoparticles

Audureau

Simon-Deckers

Franco-Montoya

et al. 2018

Sci Rep

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Anthropic nanoparticles (NP) are increasingly produced and emitted, with accompanying concerns for human health. Currently there is no global understanding as to the exact mechanistics of NP toxicity, as the traditional nanotoxicological approaches only provide a restricted overview. To address this issue, we performed an in-depth transcriptomic analysis of human macrophages exposed to a panel of welding-related metal oxide NP that we previously identified in welders lungs (Fe2O3, Fe3O4, MnFe2O4 and CrOOH NP). Utilizing the specified analysis criteria (|fold change| ≥1.5, p ≤ 0.001), a total of 2164 genes were identified to be differentially expressed after THP-1 macrophage exposure to the different NP. Performing Gene Ontology enrichment analysis, for cellular content, biological processes and Swiss-Prot/Protein Information Resource keywords the data show for the first time a profound modification of gene differential expression in response to the different NP, among which MnFe2O4 NP were the most potent to induce THP-1 macrophage activation. The transcriptomic analysis utilized in the study, provides novel insights into mechanisms that could contribute to NP-induced adverse effects and support the need for widened approaches to supplement existing knowledge of the processes underlying NP toxicity which would have not been possible using traditional nanotoxicological studies.

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“…Moreover, PM could cause systemic inflamation and influence cytokine levels in the circulation [18,19]. Some pro-inflammatory cytokines, such as TNF-α and IL-6, were detected in the joint region and plasma or serum, and they are linked to OA [56,59,60].…”

Section: Discussionmentioning

confidence: 99%

Particulate matter exposure aggravates osteoarthritis severity

et al. 2019

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Several diseases have been linked to particulate matter (PM) exposure. Outdoor activities, such as road running or jogging, are popular aerobic exercises due to few participatory limitations. Osteoarthritis (OA) is a progressive degenerative joint disease, usually observed at age 40, and not noticed before pain or diagnosis. Although exercise has health benefits, it is unclear whether outdoor jogging in higher PM (standard reference material 1649b, SRM 1649b) concentration environments could affect OA development or severity. Hence, a PM exposure monosodium iodoacetate (MIA)-induced OA animal jogged model was established for investigation. Results showed that high doses of PM (5 mg) significantly increased pro-inflammatory factors such as tumor necrosis factor α (TNF-α), interleukin (IL)-1β, and IL-6, and M1 macrophages in the lung region, also obtained in systemic IL-6 and TNF-α expressions in this MIA-OA rat model. Moreover, levels of osteocalcin, cartilage oligomeric matrix protein (COMP), and N‐telopeptides of type I collagen were especially influenced in MIA+PM groups. Morphological and structural changes of the knee joint were detected by micro-computed tomography images (micro-CT) and immunohistochemistry. MIA + PM rats exhibited severe bone density decrease, cartilage wear, and structure damages, accompanied by lower levels of physical activity, than the sham group and groups receiving MIA or PM alone. The findings suggest that the severity of OA could be promoted by PM exposure with a PM concentration effect via systemic inflammatory mechanisms. To the best of our knowledge, this is the first study to provide direct effects of PM exposure on OA severity.

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Predictive and Prognostic Biomarkers of Respiratory Diseases due to Particulate Matter Exposure

Cited by 76 publications

References 96 publications

Evidence for the critical role of the PI3K signaling pathway in particulate matter-induced dysregulation of the inflammatory mediators COX-2/PGE2 and the associated epithelial barrier protein Filaggrin in the bronchial epithelium

Evidence for the critical role of the PI3K signaling pathway in particulate matter-induced dysregulation of the inflammatory mediators COX-2/PGE2 and the associated epithelial barrier protein Filaggrin in the bronchial epithelium

Substantial modification of the gene expression profile following exposure of macrophages to welding-related nanoparticles

Particulate matter exposure aggravates osteoarthritis severity

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