Dendritic cells modulated by cytokine-expressing adenoviruses alleviate eosinophilia and airway hyperresponsiveness in an animal model of asthma Yi-Ling.

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Presentation transcript:

Dendritic cells modulated by cytokine-expressing adenoviruses alleviate eosinophilia and airway hyperresponsiveness in an animal model of asthma Yi-Ling Ye, PhD, Yueh-Lun Lee, PhD, Zen-Jai Chuang, BS, Huai-Jean Lai, MS, Chun-Chi Chen, MS, Mi-Hua Tao, PhD, Bor-Luen Chiang, MD, PhD Journal of Allergy and Clinical Immunology Volume 114, Issue 1, Pages 88-96 (July 2004) DOI: 10.1016/j.jaci.2004.03.010

Fig 1 The expression efficiency of adenovirus-infected DCs. The bold area represents the GFP expression after Ad-GL-1 infection, and the filled line represents DCs without Ad-GL-1 infection (A). Different MOI of Ad-IL-12 (B) or Ad-IL-18 (C) or 3000 MOI of Ad-IL-12 combined with different MOI of Ad-IL-18 infected DCs (D, E) were analyzed by ELISA assay. Data represent the means ± SEMs. Journal of Allergy and Clinical Immunology 2004 114, 88-96DOI: (10.1016/j.jaci.2004.03.010)

Fig 2 The cytokine levels of CD4+ positive splenocytes from cytokine gene–modulated DC treated mice. CD4+ positive cells were co-cultured with OVA and irradiated splenocytes for 48 h in 96-well culture plates and then the cultured supernatant was collected for IL-4 (A), IL-5 secretion (B), or IFN-γ (C) cytokine assay. ∗P<.05; ∗∗P<.001; each adenovirus infected group vs DCs pulsed with OVA group. Journal of Allergy and Clinical Immunology 2004 114, 88-96DOI: (10.1016/j.jaci.2004.03.010)

Fig 3 Anti-OVA antibody expression levels of DC-treated mice. The IgG2a and IgE anti-OVA antibody expression from mice that received DCs pulsed with OVA (A) or without OVA (B) was measured by ELISA and shown as pg/mL. ∗P<.05 compared with the DC pulsed OVA group; ##P<.01 compared with the Ad-IL-12 infected group. Journal of Allergy and Clinical Immunology 2004 114, 88-96DOI: (10.1016/j.jaci.2004.03.010)

Fig 4 Preventive effect of modified DCs on AHR. The value of AHR (A) was measured after the challenge, and then BAL fluid samples were collected. Cells were counted and classified as monocytes (Mon), lymphocytes (Lym), neutrophils (Neu), or eosinophils (Eos)(B). Data represent the means ± SEMs of 7-8 mice per group. ∗∗P<.01, compared with DCs pulsed with OVA group. Journal of Allergy and Clinical Immunology 2004 114, 88-96DOI: (10.1016/j.jaci.2004.03.010)

Fig 5 Inflammatory mediator levels were analyzed in BAL fluid. BAL fluid samples were collected after the challenge. Eotaxin (A), KC (B), and IL-13 (C) levels in BAL fluid from mice were measured by ELISA assay. Data represent the means ± SEMs of 5-7 mice per group. ∗P<.05, compared with DC+OVA+Ad-mock group; #P<.05, compared with DC+OVA+Ad-IL-12 group. Journal of Allergy and Clinical Immunology 2004 114, 88-96DOI: (10.1016/j.jaci.2004.03.010)

Fig 6 Histopathologic study of lung tissue in mice that received the cytokine-modulated DCs. Histopathologic changes were examined by light microscopy for DC pulsed with OVA group mice (DC+OVA), Ad-Mock (DC+OVA+Ad-mock), Ad-IL-18 (DC+OVA+Ad-18), Ad-IL-12 (DC+OVA+Ad-12), and co-infected (DC+OVA+Ad-12+Ad-18) treated mice. Data showed different extent of cellular infiltration of the periairway region. Original magnification, ×200. Journal of Allergy and Clinical Immunology 2004 114, 88-96DOI: (10.1016/j.jaci.2004.03.010)