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.
"Chronic heat stress (CHS) occurs under the high temperature conditions which are not necessarily extreme but for a long time, for example, in the hot summer. Although prolonged exposure to these environments may not be lethal, it can alter the animal's growth performance, the immune competence , and disease resistance       . Our previous studies had demonstrated that CHS significantly inhibited both systemic and local innate immune responses, including reduced numbers of pulmonary alveolar macrophages (PAMs), delayed maturation of dendritic cells (DCs), and decreased levels of IL-6, IFN-í µí»½, and HSP70 mRNA . "
[Show abstract][Hide abstract] 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.
"It has been applied to a number of viral, bacterial and parasitic disease models as well as several tumour models. There are a number of advantages on nucleic acid vaccines over conventional vaccines, such as long-term protection, long shelf life  and the ability to induce a wider range of immune response types. "
[Show abstract][Hide abstract] ABSTRACT: Foot-and-Mouth Disease (FMD), as a major global animal disease, affects millions of animals worldwide and remains the main sanitary barrier to the international and national trade of animals and animal products. Inactivated vaccination is the most effective measure for prevention of FMD at present, but fail to induce long-term protection and content new requires for production of FMD vaccines. As a number of Researchers hope to obtain satisfactory novel vaccines by new bio-technology, novel vaccines have been studied for more than thirty years. Here reviews the latest research progress of new vaccines, summarizes some importance and raises several suggestions for the future of FMD vaccine.
"In a previous study, we reported that CHS could retard the adaptive immune response by suppressing both humoral and cellular responses . In this study we have demonstrated that CHS can significantly suppress host innate immunity in mice and moderately increase the mortality of H5N1-infected mice. "
[Show abstract][Hide abstract] 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 05/2011; 2011(1110-7243):367846. DOI:10.1155/2011/367846 · 2.71 Impact Factor
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