Single-cell transcriptomics reveals the pulmonary inflammation induced by inhalation of subway fine particles.

People generally take the subway and inevitably inhale the fine particles (PM2.5) on subway platforms. This study revealed whether and how subway PM2.5 causes lung inflammation. Herein, the pulmonary inflammatory response to subway PM2.5 was observed in mice, manifesting as the inflammatory cells infiltration and collagen deposition in tissue, inflammatory cytokine enhancement in bronchoalveolar lavage fluid and Toll-like receptors signal pathway activation in the lungs. Furthermore, single-cell RNA sequencing unearthed subway PM2.5-induced cell-specific responses in the lungs. Twenty immune subsets were identified by the molecular and functional properties. Specific cell populations of CD4+ T and γδ T cells were regarded as the predominant sources of pneumonitis induced by subway PM2.5. Moreover, we demonstrated that the lung inflammatory injury was significantly more attenuated in Rag1-/- mice lacking functional T cells and B cells than that in wild type mice. We proved the slight inflammation of lung tissue in Rag1-/- mice may be dependent on monocytes and neutrophils by activation of the intracellular molecular network. This is the first experimental study on subway PM2.5 causing pulmonary inflammatory damage. It will set an alarm for people who usually travel by subway and efficient measures to reduce PM2.5 should be developed in subway stations.

Intratracheally administered iron oxide nanoparticles induced murine lung inflammation depending on T cells and B cells.

Iron oxide nanoparticles (Fe2O3 NPs), produced in track traffic system and a wide range of industrial production, poses a great threat to human health. However, there is little research about the mechanism of Fe2O3 NPs toxicity on respiratory system. Rag1-/- mice which lack functional T and B cells were intratracheally challenged with Fe2O3 NPs, and interleukin (IL)-33 as an activator of group 2 innate lymphoid cells (ILC2s) to observe ILC2s changes. The lung inflammatory response to Fe2O3 NPs was alleviated in Rag1-/- mice compared with wild type (WT) mice. Infiltration of inflammatory cells and collagen deposition in tissue, leukocyte numbers (neutrophils, macrophages and lymphocytes), cytokine levels, such as IL-6, IL-13 and thymic stromal lymphopoietin (TSLP), and expression of Toll-like receptor (TLR)2, TLR4, and downstream myeloid differentiation factor (MyD)88, nuclear factor (NF)-κB and tumor necrosis factor (TNF)-α were decreased in lungs. Fe2O3 NPs markedly elevated ILC2s compared with the control, but ILC2s numbers were much lower compared with IL-33 in both WT and Rag1-/- mice. Furthermore, ILC2s amounts were strongly greater in Rag1-/- mice than WT mice. Our results suggested that Fe2O3 NPs induced sub-chronic pulmonary inflammation, which is majorly dependent on T cells and B cells rather than ILC2s.

Inhalation of subway fine particles induces murine extrapulmonary organs damage.

Because of its speed and convenience, the subway has become the first choice for travel by many residents. However, the concentration of fine particles (PM2.5) in the air of a subway platform is higher than that of the ground level or carriage. Moreover, the composition and source of subway PM2.5 differ from those of atmospheric PM2.5. Currently, there is insufficient research on the impact of subway PM2.5 on health. In this study, intratracheally subway PM2.5-inoculated wild type (WT) and Rag1-/- mice, lacking functional T cells and B cells, were used to investigate the potential of subway PM2.5 exposure to cause extrapulmonary organ injuries. Subway PM2.5 increased inflammatory cells infiltration, tumor necrosis factor (TNF)-α, interleukin (IL)-6, as well as monocyte chemotactic protein (MCP)-1 gene and protein expression, cyclooxygenase-2 (COX-2) induction, and Toll-like receptor (TLR)-2, TLR4, myeloid differentiation factor 88 (MyD88), and nuclear factor (NF)-κB levels in liver, kidney, spleen, and thymus in a dose-dependent fashion in WT mice. Subway PM2.5 exposure resulted in slight macrophage (F4/80+) and neutrophil (Ly6G+) infiltration and caused no increase in the protein levels of TNF-α, IL-6, MCP-1, or COX-2 in the liver, kidneys, spleen, and thymus of Rag1-/- mice. These results demonstrate a dose-response manner between subway PM2.5 exposure and inflammatory injuries of extrapulmonary organs, which could be related to the TLR/MyD88/NF-κB signaling pathway. Subway PM2.5-induced extrapulmonary organ damage was dependent on T cells and B cells; this finding may provide insight for research on the mechanisms responsible for the health hazards posed by air pollution.

Phytochemical Constituents and Antiproliferative Activities of Essential Oils from Four Varieties of Malaysian Zingiber officinale Roscoe against Human Cervical Cancer Cell Line.

This study evaluates the volatile metabolic constituents and anticancer potential of essential oils distilled from the rhizomes of four Malaysian Zingiber officinale Roscoe (Zingiberaceae family) varieties (Bentong (BE), Cameron Highlands (CH), Sabah (SA), and Bara (BA)). The ginger essential oils were analyzed by gas chromatography coupled with quadrupole mass spectrometry (GC qMS). A total of 58 secondary compounds were tentatively identified, representing 82.6-87.4% of the total ion count. These metabolites comprise mainly of monoterpene hydrocarbons (19.7-25.5%), oxygenated monoterpenes (23.6-33.7%), sesquiterpene hydrocarbons (21.3-35.6%), oxygenated sesquiterpenes (1.5-3.9%), and other minor classes of compounds (0.7-2.7%). Principal component analysis (PCA) enabled differentiation of the analyzed ginger essential oils according to their varieties, with respect to their metabolites and relative quantities. The antiproliferative activity against the HeLa cervical cancer cell line was investigated via the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The oils were found to exhibit strong antiproliferative activities with IC50 values of 23.8, 35.3, 41.3, and 42.5 µg/mL for BA, BE, SA, and CH, respectively. These findings suggest that the differences among the secondary metabolites and their abundance in different varieties of Z. officinale essential oils appear to be related to their antiproliferative potential. The strong antiproliferative effects of these oils signified their potential in the prevention and chemotherapy of cervical carcinoma treatment.