Effects of chronic heat stress on immune responses of the foot-and-mouth disease DNA vaccination.
ABSTRACT The main purpose of this study was to assess the effects of chronic heat stress (CHS) on humoral and cellular responses of DNA vaccination. Mice with the CHS were exposed to a temperature set at 38 +/- 1 degrees C, 2h per day, for 35 days, and mice with thermoneutral (TN) temperature were maintained at 24 +/- 1 degrees C for the same period of time. Both groups of mice were immunized with a DNA vaccine-expressed viruscapsid protein 1 (VP1) of foot-and-mouth disease virus (FMDV), and we tested their antigen-specific humoral and cellular responses during the treatments. Compared with the TN group, titers of total Imunoglobulin G (IgG) and IgG1 and expression of interleukin 4 (IL-4) in CD4(+) cells of CHS group were not affected significantly. In contrast, the levels of IgG2a, T cell proliferations, and expression of interferon-gama (IFN-gamma) in both CD4(+) and CD8(+) cells were suppressed significantly, and cytotoxic T-lymphocyte (CTL) responses in vivo were also weakened by the CHS condition. These results indicate that the CHS treatment has negatively affected the immune responses of DNA vaccination and particularly impaired to the cell-mediated responses. It suggests that vaccination in animals is affected by the changes of ambient temperature.
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ABSTRACT: Chronic heat stress (CHS) can negatively affect immune response in animals. In this study we assessed the effects of CHS on host innate immunity and avian influenza virus H5N1 infection in mice. Mice were divided into two groups: CHS and thermally neutral (TN). The CHS treatment group exhibited reduced local immunity in the respiratory tract, including the number of pulmonary alveolar macrophages and lesions in the nasal mucosa, trachea, and lungs. Meanwhile, CHS retarded dendritic cells (DCs) maturation and reduced the mRNA levels of IL-6 and IFN-β significantly (P < .05). After the CHS treatment, mice were infected with H5N1 virus. The mortality rate and viral load in the lungs of CHS group were higher than those of TN group. The results suggest that the CHS treatment could suppress local immunity in the respiratory tract and innate host immunity in mice significantly and moderately increased the virulence in H5N1-infected mice.BioMed Research International 01/2011; 2011:367846. · 2.71 Impact Factor
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ABSTRACT: Plasmacytoid dendritic cells (pDCs) play a crucial role in anti-viral immunity through production of large amounts of interferons (IFNs). A previous study revealed the existence of lactic acid bacteria that directly stimulate pDCs in mice. In this study, we demonstrated that Lactococcus lactis JCM5805 activates human pDCs and induces IFN production in vitro. In addition, our randomized, placebo-controlled, double blind test showed that yogurt fermented with L. lactis JCM5805 activated pDC activity in vivo. This effect was greater in low pDC subjects, and their ability to produce IFNs was increased from the beginning. Furthermore, the risk of morbidity from the common cold was suppressed in the L. lactis JCM5805 group compared with the placebo group. In conclusion, intake of L. lactis JCM5805 can directly activate pDCs and increase the ability to produce IFNs in vivo. Therefore, L. lactis JCM5805 may be a beneficial tool to enhance anti-viral immunity in humans.Clinical Immunology 10/2013; 149(3PB):509-518. · 3.77 Impact Factor
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ABSTRACT: Chronic heat stress (CHS) is known to have negative impacts on the immune responses in animals and increases their susceptibility to infections including the highly pathogenic avian influenza virus H5N1. However, the role of regulatory T cells (Tregs) in CHS immunosuppression remains largely undefined. In this study, we demonstrated a novel mechanism by which CHS suppressed both Th1 and Th2 immune responses and dramatically decreased the protective efficacy of the formalin-inactivated H5N1 vaccine against H5N1 influenza virus infection. This suppression was found to be associated with the induced generation of CD4(+)CD25(+)FoxP3(+) Tregs and the increased secretions of IL-10 and TGF- β in CD4(+) T cells. Adoptive transfer of the induced Tregs also suppressed the protective efficacy of formalin-inactivated H5N1 virus immunization. Collectively, this study identifies a novel mechanism of CHS immunosuppression mediated by regulating CD4(+)CD25(+)Foxp3(+) Tregs.BioMed research international. 01/2013; 2013:160859.