34 research outputs found
PM<sub>2.5</sub> exposure exacerbated airway inflammatory cell infiltration in mice with OVA induced pre-existing asthma.
<p>(A) Histopathological examination of lung tissue inflammatory cell infiltration in mice. Representative photos of H&E-stained lung sections (original magnification 20x). (B) Cell population of macrophage, eosinophil, neutrophil and lymphocyte in BALF. Each value is expressed as mean ± SEM. n = 5–8. * <i>P</i>< 0.05, ** <i>P</i> < 0.005, *** <i>P</i> < 0.001 vs. CON; <sup>+</sup> <i>P</i> < 0.05 vs. OVA+FILTER.</p
Experimental setup of the PM<sub>2.5</sub> exposure enhanced mouse model of asthma.
<p>Experimental setup of the PM<sub>2.5</sub> exposure enhanced mouse model of asthma.</p
Oral administration of <i>Lactobacillus paracasei</i> L9 attenuates PM<sub>2.5</sub>-induced enhancement of airway hyperresponsiveness and allergic airway response in murine model of asthma
<div><p>This study investigated allergy immunotherapy potential of <i>Lactobacillus paracasei</i> L9 to prevent or mitigate the particulate matter 2.5 (PM<sub>2.5</sub>) enhanced pre-existing asthma in mice. Firstly, we used a mouse model of asthma (a 21-day ovalbumin (OVA) sensitization and challenge model) followed by PM<sub>2.5</sub> exposure twice on the same day of the last challenge. PM<sub>2.5</sub> was collected from the urban area of Beijing and underwent analysis for metals and polycyclic aromatic hydrocarbon contents. The results showed that PM<sub>2.5</sub> exposure enhanced airway hyper-responsiveness (AHR) and lead to a mixed Th2/ IL-17 response in asthmatic mice. Secondly, the PM<sub>2.5</sub> exposed asthmatic mice were orally administered with L9 (4×10<sup>7</sup>, 4×10<sup>9</sup> CFU/mouse, day) from the day of first sensitization to the endpoint, for 20 days, to investigate the potential mitigative effect of L9 on asthma. The results showed that L9 ameliorated PM<sub>2.5</sub> exposure enhanced AHR with an approximate 50% decrease in total airway resistance response to methacholine (48 mg/ml). L9 also prevented the exacerbated eosinophil and neutrophil infiltration in bronchoalveolar lavage fluid (BALF), and decreased the serum level of total IgE and OVA-specific IgG1 by 0.44-fold and 0.3-fold, respectively. Additionally, cytokine production showed that L9 significantly decreased T-helper cell type 2 (Th2)–related cytokines (IL-4, -5, -13) and elevated levels of Th1 related IFN-γ in BALF. L9 also reduced the level of IL-17A and increased the level of TGF-β. Taken together, these results indicate that L9 may exert the anti-allergic benefit, possibly through rebalancing Th1/Th2 immune response and modulating IL-17 pro-inflammatory immune response. Thus, L9 is a promising candidate for preventing PM exposure enhanced pre-existing asthma.</p></div
MOESM1 of Interaction of γ-Fe2O3 nanoparticles with Citrus maxima leaves and the corresponding physiological effects via foliar application
Additional file 1: Figure S1. (A) TEM image showing the morphology of the suspension of γ-Fe2O3 NPs in deionized water. DLS analysis showing (B) size distribution and (C) zeta potential of γ-Fe2O3 NPs in deionized water
PM<sub>2.5</sub> exposure exacerbated systemic and airway allergic response in mice with OVA induced pre-existing asthma.
<p>(A) Serum levels of immunoglobulin production. (B) Cytokines production in BALF. Each value is expressed as mean ± SEM. n = 5–8. * <i>P</i>< 0.05, ** <i>P</i> < 0.005, *** <i>P</i> < 0.001 vs. CON; <sup>+</sup> <i>P</i> < 0.05 vs. OVA+FILTER.</p
Analysis of Metal and PAH composition in PM<sub>2.5</sub>.
<p>Analysis of Metal and PAH composition in PM<sub>2.5</sub>.</p
PM<sub>2.5</sub> exposure exacerbated AHR in mice with OVA induced pre-existing asthma.
<p>(A) AHR to increasing doses of Mch. (B) The maximal response to Mch challenge. Each value is expressed as mean ± SEM. N = 5–8. * <i>P</i>< 0.05, ** <i>P</i> < 0.005, *** <i>P</i> < 0.001 vs. CON; <sup>+</sup> <i>P</i> < 0.05 vs. OVA+FILTER.</p
Administration of L9 ameliorated AHR enhanced by exposure of PM<sub>2.5</sub>.
<p>(A) AHR to increasing doses of Mch. (B) The maximal response to Mch challenge. Each value is expressed as mean ± SEM. n = 5–8. ## <i>P</i> < 0.005, ### <i>P</i> < 0.001 vs. OVA+PM<sub>2.5</sub>.</p
Administration of L9 prevented exacerbated inflammatory cell infiltration induced by exposure of PM<sub>2.5</sub>.
<p>(A) Histopathological examination of lung tissue inflammatory cell infiltration in mice. Representative photos of H&E-stained lung sections (original magnification 20x). (B) Cell population of macrophage, eosinophil, neutrophil and lymphocyte in BALF. Each value is expressed as mean ± SEM. n = 5–8. ## <i>P</i> < 0.005, ### <i>P</i> < 0.001 vs. OVA+PM<sub>2.5</sub>.</p
Administration of L9 attenuated the mixed allergic response induced by exposure of PM<sub>2.5</sub>.
<p>(A) Serum levels of immunoglobulin production. (B) Cytokines production in BALF. Each value is expressed as mean ± SEM. n = 5–8. # <i>P</i> < 0.05, ## <i>P</i> < 0.005, ### <i>P</i> < 0.001 vs. OVA+PM<sub>2.5</sub>.</p