Biomedical subjects

Yi-Ling Ye

Publications and source records attributed to Yi-Ling Ye.

3 recordsLinked to original sources

PubMed2003

Ribavirin or CpG DNA sequence-modulated dendritic cells decrease the IgE level and airway inflammation.

Asthma is an allergic disease that is characterized by the imbalance between Th1 and Th2 cells and by the predominant Th2-type immune response. In this study, we investigated the application of dendritic cell (DCs)-based immunotherapy in modulating the immune response of allergic diseases. DCs incubated with ovalbumin (OVA), OVA plus ribavirin, OVA plus CpG-oligodeoxynucleotides (ODN 1826), or OVA plus non-CpG-ODN (ODN 1745) for 48 hours were injected intravenously into four corresponding groups of BALB/c mice. All of the mice were then immunized with OVA intraperitoneally 7 days later to establish an animal model of asthma. Serum levels of OVA antibody, airway hyperresponsivness, cell composition and cytokine levels in the bronchoalveolar lavage fluid, and cytokine profiles of spleen cells were analyzed. The data showed that ribavirin and ODN 1826 increased interleukin-12 synthesis and inhibited interleukin-10 production. ODN 1826 could also enhance the expression of B7.1, B7.2, major histocompatibility complex I, and major histocompatibility complex II molecules. Furthermore, the DCs modulated by ribavirin and ODN 1826 could downregulate the Th2-type immune response in vivo and could alleviate airway inflammation. This study elucidated the effect of ribavirin and CpG-ODN on DCs and demonstrated that in vitro modulated DCs might be a potential therapeutic approach for asthma.

Adjuvants, Immunologic↗

PubMed2003

Both allergen-specific CD4 and CD8 Type 2 T cells decreased in asthmatic children with immunotherapy.

Allergen-specific immunotherapy (IT) has been used for the treatment of atopic diseases since the turn of this century. The precise working mechanisms, however, remain to be clarified. The aim of this study was to investigate the role of particular subsets of allergen-specific T cells in the non-atopic individuals, untreated asthmatic children and the asthmatic children receiving immunotherapy. We collected peripheral blood from 16 untreated asthmatic children and 17 asthmatic children receiving immunotherapy over one and half years. All the patients were sensitive to mite allergen. Peripheral blood mononuclear cells (PBMC) were isolated and, in vitro, stimulated with crude mite extract to enrich the mite-specific T-cell population. After 14 days, the enriched mite-specific T cells were stimulated with phorbol-12-myristate-13-acetate (PMA) and ionomycin for intracellular detection of cytokines such as IFN-gamma, IL-4 in CD4+ and CD8+ T lymphocytes. The data here demonstrated that the levels of mite-specific IgG4 and IgA increased significantly in asthmatic children after immunotherapy. In addition, both IL-4 expressing CD4+ and CD8+ T cells were significantly lower in asthmatic children after immunotherapy compared with those of before treatment and the normal control (p < 0.05). In contrast, the frequency of IFN-gamma expressing CD4+ and CD8+ T cells did not significantly differ between untreated and SIT-treated groups. All these data suggested that decreased Type 2 CD4+ and CD8+ T cells might be closely correlated with the regulatory mechanisms of immunotherapy.

Adolescent↗

PubMed2002

Interleukin-12 inhibits eotaxin secretion of cultured primary lung cells and alleviates airway inflammation in vivo.

The mechanisms that cause the inflammation of airway and lung tissue in asthma have been studied extensively. It is noted that type 1T helper cell (Th1)-related cytokines could decrease the accumulation of eosinophils in lung tissue and relieve airway constriction. But the therapeutic mechanisms of Th1 cytokines remain unclear. In this study, interleukin-12 (IL-12) DNA plasmid as a therapeutic reagent was delivered intravenously. Bronchoalveolar lavage (BAL) fluids were collected from IL-12 treated and control mice, and analyzed for cell composition and eotaxin level. The results showed that IL-12 DNA plasmid could effectively inhibit eosinophilia and airway inflammation in vivo. The level of eotaxin in BAL fluid also decreased. To further investigate the effect of Th1-related cytokines such as IL-12 or interferon-gamma (IFN-gamma) on the eotaxin level produced by lung cells, primary lung cell culture was established. The results demonstrated that both IL-12 and IFN-gamma could suppress eotaxin secretion from IL-13 or IL-4 stimulated primary lung cell culture. Moreover, the inhibitory effect of IL-12 could not be reversed by the administration of anti-IFN-gamma antibody. All the evidences suggested that IL-12 could regulate airway inflammation by suppressing the eotaxin secretion of lung tissue through an IFN-gamma independent mechanism.

Animals↗