Abstract

BackgroundMycoplasma hyopneumoniae (Mhp) causes porcine enzootic pneumonia, a disease that cause major economic losses in the pig industry. Dendritic cells (DCs), the most effective antigen-presenting cells, are widely distributed beneath respiratory epithelium, DCs uptake and present antigens to T cells, to initiate protective immune responses in different infections. In this study, we investigated the role of porcine DCs in vaccine Mhp-168 exposure.ResultsThe antigen presenting ability of DCs were improved by vaccine Mhp-168 exposure. DCs could activate T-cell proliferation by up-regulating the antigen presenting molecule MHCII expression and co-stimulatory molecule CD80/86. However, the up-regulation of IL-10 and accompany with down-regulation of IFN-γ gene level may account for the limitation of attenuated Mhp-168 strain use as vaccine alone.ConclusionThese findings are benefit for exploring the protection mechanisms and the possible limitations of this attenuated Mhp-168 vaccine.

Highlights

  • Mycoplasma hyopneumoniae (Mhp) causes porcine enzootic pneumonia, a disease that cause major economic losses in the pig industry

  • Morphology of bone marrow-derived Dendritic cells (DCs) (BMDCs) after 6 days culture Bone marrow-derived cells were cultured for 6 days by using RPMI 1640 media with granulocyte-macrophage colony-stimulating factor (GM-CSF) and rpIL-4 to allow them to differentiate into immature BMDCs

  • Phenotypic alteration of BMDCs stimulated by vaccine Mhp-168 in vitro DCs phenotypic maturation is essential for T cells activation and immune response

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Summary

Introduction

Mycoplasma hyopneumoniae (Mhp) causes porcine enzootic pneumonia, a disease that cause major economic losses in the pig industry. Mycoplasma hyopneumoniae (Mhp) causes porcine enzootic pneumonia (EP) and causes tremendous economic losses all over the swine industry [1]. Mhp infection causes physical damage on the respiratory tract and modulates the host immune response [3], the primary Mhp infection often becomes complicated by secondary bacterial and viral infections [4]. Mhp infection causes the release of inflammatory cytokines, such as interleukin (IL)-1β, IL18 both in vivo and in vitro [5]. The lower respiratory tract (trachea and lung) is essentially sterile, pathogenic microorganisms have the opportunity to colonize and invade the host when the cilia clearance ability is impaired [6].

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