Inflammatory cell profiles in BALF following the 2^nd exposure to PM.

<p>Inflammatory cell profiles in BALF following the 2^nd exposure to PM.</p

The effect of size-segregated ambient particulate matter on Th1/Th2-like immune responses in mice

<div><p>Background</p><p>Particulate matter (PM) has been associated with increased pulmonary and cardiovascular mortality and morbidity. Additionally, PM is known to exacerbate asthma. However, whether ambient PM exposure contributes to the onset of asthma, especially in non-atopic children and adults, is less conclusive. The current study aimed to evaluate the effects of size-fractioned PM on lung immune responses in healthy BALB/c mice.</p><p>Methods and principal findings</p><p>We collected PM₁₀, PM_2.5, PM₁ and PM_0.1 samples from October 2012 to August 2013 in the Taipei Basin. These PM samples were representative of urban traffic pollution. The samples were extracted and sonicated in phosphate-buffered saline (PBS). Female BALB/c mice were exposed to the samples via intratracheal instillation at three different doses: 1.75 mg/kg (35 μg/per mouse), 5 mg/kg (100 μg/per mouse), and 12.5 mg/kg (250 μg/per mouse). The mice were exposed on days 0 and 7, and PBS alone was used as a control. Following the exposures, the expression profiles of inflammatory cells and cytokines in bronchoalveolar lavage fluid (BALF) were assessed. Exposure to PM₁₀ resulted in inflammatory responses, including the recruitment of neutrophils and the induction of T helper 1 (Th1) cell-related cytokine release, such as TNF-α and IFN-γ. Furthermore, an allergic immune response, including the recruitment of eosinophils and the up-regulation of T helper 2 (Th2) cell-related cytokine release, such as IL-5 and IL-13, was also observed in the BALF of mice exposed to PM₁₀.</p><p>Conclusions</p><p>Our study showed that exposure to PM alone caused mixed Th1/Th2 inflammatory responses in healthy mice. These findings support the hypothesis that PM may contribute to the onset of asthma.</p></div

Representative histology of lung tissue (200X) 3 days after the second intratracheal instillation of PM.

<p>Lungs were excised and fixed with formaldehyde, sectioned in 5-μm-thick slices, and the slides were stained with H&E. (A) Vehicle (VEH) control tissue. (B) Tissue exposed to high-dose PM_2.5 showing focal aggregation of lymphocytes and foamy histiocytes in the alveolar space. (C) Tissue exposed to medium-dose PM₁₀ showing focal infiltration of lymphocytes and foamy histiocytes into the alveolar space. (D) Tissue exposed to high-dose PM₁₀ showing focal infiltration of neutrophils, lymphoplasma cells and foamy histiocytes.</p

Coefficients for the correlations between the constituents in the PM samples and the measured inflammatory responses.

<p>Coefficients for the correlations between the constituents in the PM samples and the measured inflammatory responses.</p

Overview of the experimental design used to expose mice to PM.

<p>Mice (10–15 animals per group) were divided into the following five groups: PBS, PM_0.1, PM₁, PM_2.5, and PM₁₀. Each group was further divided according to dose: either two or three doses of 1.75 mg/kg (35 μg/per mouse), 5 mg/kg (100 μg/per mouse) or 12.5 mg/kg (250 μg/per mouse) were administered. On days 0 and 7, the mice were exposed to 100 μL of the appropriate solution by intratracheal instillation under light anesthesia. The animals were sacrificed 3 days after the second treatment, and samples of blood, BALF and lung were collected.</p

Cytokine levels in BALF following the 2^nd exposure to PM.

<p>A: IFN-γ. B: IL-5. C: IL-6. D: IL-13. E: IL-17A. F: TNF-α. The mice were exposed to 100 μL aliquots of solutions by intratracheal instillation on days 0 and 7 as described in the <i>Materials and Methods</i> section. PBS served as a vehicle control. The data are presented as the mean ± SEM (n = 5 per treatment group). *<i>p</i><0.05 compared to the PBS control group; ^#<i>p</i><0.05 compared to the other groups at the same dose.</p

Serum total IgE, serum IL-6 and total protein in BALF.

<p>Serum total IgE, serum IL-6 and total protein in BALF.</p

Inflammatory cell profiles in BALF following the 2^nd exposure to PM.

<p>A: Total cells. B: Neutrophils. C: Lymphocytes. D: Eosinophils. The mice were exposed to 100 μL aliquots of solutions by intratracheal instillation on days 0 and 7 as described in the <i>Materials and Methods</i> section. The data are presented as the mean ± SEM (n = 5 per treatment group). Neutrophil, lymphocyte and eosinophil counts are expressed as percentages of total cell counts. *<i>p</i><0.05 compared to the PBS group; ^#<i>p</i><0.05 compared to the other groups at the same dose.</p

Chemical mass constituents in size-segregated ambient PM collected between the 2012 winter and 2013 summer seasons.

<p>Chemical mass constituents in size-segregated ambient PM collected between the 2012 winter and 2013 summer seasons.</p

Thickness-Dependent Binding Energy Shift in Few-Layer MoS₂ Grown by Chemical Vapor Deposition

The thickness-dependent surface states of MoS₂ thin films grown by the chemical vapor deposition process on the SiO₂–Si substrates are investigated by X-ray photoelectron spectroscopy. Raman and high-resolution transmission electron microscopy suggest the thicknesses of MoS₂ films to be ranging from 3 to 10 layers. Both the core levels and valence band edges of MoS₂ shift downward ∼0.2 eV as the film thickness increases, which can be ascribed to the Fermi level variations resulting from the surface states and bulk defects. Grainy features observed from the atomic force microscopy topographies, and sulfur-vacancy-induced defect states illustrated at the valence band spectra imply the generation of surface states that causes the downward band bending at the n-type MoS₂ surface. Bulk defects in thick MoS₂ may also influence the Fermi level oppositely compared to the surface states. When Au contacts with our MoS₂ thin films, the Fermi level downshifts and the binding energy reduces due to the hole-doping characteristics of Au and easy charge transfer from the surface defect sites of MoS₂. The shift of the onset potentials in hydrogen evolution reaction and the evolution of charge-transfer resistances extracted from the impedance measurement also indicate the Fermi level varies with MoS₂ film thickness. The tunable Fermi level and the high chemical stability make our MoS₂ a potential catalyst. The observed thickness-dependent properties can also be applied to other transition-metal dichalcogenides (TMDs), and facilitates the development in the low-dimensional electronic devices and catalysts