53 research outputs found

    Protein−protein interaction network for differentially colostral whey proteins between mothers with or without gestational hypothyroidism.

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    Proteins up-regulated in the G-HypoT group were labeled with up red arrows, and down-regulated proteins were labeled with down blue arrows.</p

    Western blot validation.

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    (A) cell structural proteins between two groups from three individual donors. (B) complement proteins between two groups from three individual donors. C3, complement C3; C4b, complement C4b; CFH, complement factor H.</p

    PM<sub>2.5</sub> exposure exacerbated airway inflammatory cell infiltration in mice with OVA induced pre-existing asthma.

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    <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

    Hierarchical clustering of differentially expressed colostral whey proteins between mothers with or without gestational hypothyroidism.

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    Bar color represents a logarithmic scale from −0.4 to 0.4. Red indicates higher expression and green indicates lower expression.</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

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    <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

    Different protein classifications and western blot validation.

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    (A) Functional categorization of 44 proteins identified in the significance analyses. (B) Subcellular location of all 44 proteins identified in the significance analyses. The number of proteins in each category is indicated in parentheses. Enrichment analysis of differentially expressed proteins (C) Gene ontology (D) KEGG pathway.</p
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