Eine Plattform für die Wissenschaft: Bauingenieurwesen, Architektur und Urbanistik
Saharan dust induces the lung disease-related cytokines granulocyte–macrophage colony-stimulating factor and granulocyte colony-stimulating factor
Graphical abstract Display Omitted
Highlights RNA sequencing was applied to an alveolar air–liquid interface co-culture model. Different inflammatory mediators were activated by Saharan dust and quartz dust. Saharan dust induced the lung disease-related cytokines GM-CSF and G-CSF.
Abstract Desert dust exposure is associated with adverse respiratory health effects. Desert dust is a complex pollutant mixtures that includes respirable crystalline and amorphous particles, metals, and microbial constituents. Given the health effects of desert dust and its heterogeneity, as yet unidentified harmful biological pathways may be triggered. Therefore, we exposed human in vitro air–liquid interface co-cultures of alveolar epithelial A549 cells and THP-1 macrophages to Saharan dust (SD). For comparison, we used the known pulmonary toxicant DQ12 quartz dust. Via RNA sequencing, we identified that SD but not DQ12 increased the gene expression of granulocyte–macrophage colony-stimulating factor (GMCSF) and granulocyte colony-stimulating factor (GCSF). These findings were confirmed by quantitative reverse transcriptase PCR. SD dose-dependently upregulated GMCSF and GCSF expression with significant 7 and 9-fold changes, respectively, at the highest tested concentration of 31 µg/cm2. Furthermore, we observed that SD significantly enhanced the secretion of GM-CSF and G-CSF by 2-fold. Both cytokines have previously been associated with lung diseases such as asthma and fibrosis. Hence, we present two molecular messengers that may contribute to the adverse health effects of desert dust and might serve as drug targets for this globally relevant non-anthropogenic air pollutant.
Saharan dust induces the lung disease-related cytokines granulocyte–macrophage colony-stimulating factor and granulocyte colony-stimulating factor
Graphical abstract Display Omitted
Highlights RNA sequencing was applied to an alveolar air–liquid interface co-culture model. Different inflammatory mediators were activated by Saharan dust and quartz dust. Saharan dust induced the lung disease-related cytokines GM-CSF and G-CSF.
Abstract Desert dust exposure is associated with adverse respiratory health effects. Desert dust is a complex pollutant mixtures that includes respirable crystalline and amorphous particles, metals, and microbial constituents. Given the health effects of desert dust and its heterogeneity, as yet unidentified harmful biological pathways may be triggered. Therefore, we exposed human in vitro air–liquid interface co-cultures of alveolar epithelial A549 cells and THP-1 macrophages to Saharan dust (SD). For comparison, we used the known pulmonary toxicant DQ12 quartz dust. Via RNA sequencing, we identified that SD but not DQ12 increased the gene expression of granulocyte–macrophage colony-stimulating factor (GMCSF) and granulocyte colony-stimulating factor (GCSF). These findings were confirmed by quantitative reverse transcriptase PCR. SD dose-dependently upregulated GMCSF and GCSF expression with significant 7 and 9-fold changes, respectively, at the highest tested concentration of 31 µg/cm2. Furthermore, we observed that SD significantly enhanced the secretion of GM-CSF and G-CSF by 2-fold. Both cytokines have previously been associated with lung diseases such as asthma and fibrosis. Hence, we present two molecular messengers that may contribute to the adverse health effects of desert dust and might serve as drug targets for this globally relevant non-anthropogenic air pollutant.
Saharan dust induces the lung disease-related cytokines granulocyte–macrophage colony-stimulating factor and granulocyte colony-stimulating factor
Bredeck, Gerrit (Autor:in) / Dobner, Jochen (Autor:in) / Rossi, Andrea (Autor:in) / Schins, Roel P.F. (Autor:in)
14.03.2024
Aufsatz (Zeitschrift)
Elektronische Ressource
Englisch
ALI , air-liquid interface , <italic>CCL3L1</italic> , C-C motif chemokine ligand<hsp></hsp>3 like<hsp></hsp>1 , CXCL , C-X-C motif chemokine ligand , DEG , differentially expressed gene , ELISA , enzyme-linked immunosorbent assay , <italic>GCSF</italic>/G-CSF , granulocyte colony-stimulating factor , <italic>GMCSF</italic>/GM-CSF , granulocyte-macrophage colony-stimulating factor , GSEA , gene set enrichment analysis , IL , interleukin , LPS , lipopolysaccharide , qRT-PCR , quantitative reverse transcriptase polymerase chain reaction , SD , Saharan dust , <italic>SLC39A8</italic> , solute carrier family 39 member 8 , TNF , tumor necrosis factor , African dust , Mineral dust , Crystalline silica , Colony-stimulating factor 2 , Colony-stimulating factor 3 , Pulmonary disease