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Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Infection Induced Apoptosis and Autophagy in Thymi of Infected Piglets.

Wang G, Yu Y, Tu Y, Tong J, Liu Y, Zhang C, Chang Y, Wang S, Jiang C, Zhou EM, Cai X - PLoS ONE (2015)

Bottom Line: These findings demonstrated that HP-PRRSV induces apoptosis in bystander cells, and induces autophagy in both infected and bystander cells in the thymus of infected piglets.Herein, we first present new data on the thymic lesions induced by HP-PRRSV, and show that apoptosis and autophagy are key mechanisms involved in cell survival and determinants of the severity of thymic atrophy in infected piglets.Finally, future studies of the mechanism underlying immune responses are proposed based on our current understanding of PRRSV-host interactions.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, 150001, PR China.

ABSTRACT
Previously, we demonstrated that the highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) HuN4 strain causes obvious thymic atrophy and thymocytes apoptosis in infected piglets after birth, which is more severe than that induced by classical PRRSV. In this study, we investigated apoptosis and autophagy in the thymus of piglets infected with the HP-PRRSV HuN4 strain, and found that both apoptosis and autophagy occurred in the thymus of piglets infected with HP-PRRSV. In addition to a few virus-infected cells, CD14+ cells, the main autophagic cells in the thymus were thymic epithelial cells. These findings demonstrated that HP-PRRSV induces apoptosis in bystander cells, and induces autophagy in both infected and bystander cells in the thymus of infected piglets. Herein, we first present new data on the thymic lesions induced by HP-PRRSV, and show that apoptosis and autophagy are key mechanisms involved in cell survival and determinants of the severity of thymic atrophy in infected piglets. Finally, future studies of the mechanism underlying immune responses are proposed based on our current understanding of PRRSV-host interactions.

No MeSH data available.


Related in: MedlinePlus

Colocalization of CD3+ cells, CD14+ cells, thymic epithelial cells, and autophagic cells.CD3+ cells were stained with spectral red (SPRD)-conjugated mouse anti-pig CD3 antibodies, and autophagic cells were stained with anti-LC3 primary antibodies and anti-rabbit secondary antibodies conjugated to FITC, no CD3+ cells underwent autophagy (A); CD14+ cells were stained with FITC-conjugated mouse anti-pig CD14 antibodies and autophagic cells were stained with anti-LC3 primary antibodies and TRITC-conjugated goat anti-mouse antibodies, some CD14+ cells underwent autophagy (arrows) (B). Thymic epithelial cells were stained with mouse anti-pan-cytokeratin (P-CK) antibodies and FITC-conjugated goat anti-mouse antibodies, and autophagic cells were stained with anti-LC3 primary antibodies and TRITC-conjugated goat anti-mouse antibodies, most autophagic cells colocalized with thymic epithelial cells (arrows) (C). Nuclei were stained with DAPI.
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pone.0128292.g004: Colocalization of CD3+ cells, CD14+ cells, thymic epithelial cells, and autophagic cells.CD3+ cells were stained with spectral red (SPRD)-conjugated mouse anti-pig CD3 antibodies, and autophagic cells were stained with anti-LC3 primary antibodies and anti-rabbit secondary antibodies conjugated to FITC, no CD3+ cells underwent autophagy (A); CD14+ cells were stained with FITC-conjugated mouse anti-pig CD14 antibodies and autophagic cells were stained with anti-LC3 primary antibodies and TRITC-conjugated goat anti-mouse antibodies, some CD14+ cells underwent autophagy (arrows) (B). Thymic epithelial cells were stained with mouse anti-pan-cytokeratin (P-CK) antibodies and FITC-conjugated goat anti-mouse antibodies, and autophagic cells were stained with anti-LC3 primary antibodies and TRITC-conjugated goat anti-mouse antibodies, most autophagic cells colocalized with thymic epithelial cells (arrows) (C). Nuclei were stained with DAPI.

Mentions: Previously, we characterized HuN4-infected cells, which were CD14+ cells, and apoptotic cells, which were mainly CD3+ cells [21]. Here, to characterize the types of thymic cells undergoing autophagy, CD14+ cells were also stained with FITC-conjugated mouse anti-pig CD14 antibodies, CD3+ cells were stained with spectral red (SPRD)-conjugated mouse anti-pig CD3 antibodies, and thymic epithelial cells were stained with mouse anti-pan-cytokeratin (P-CK) antibodies and FITC-conjugated goat anti-mouse antibodies. LC3 was strained using both anti-LC3 polyclonal antibody and FITC/TRITC-conjugated goat anti-rabbit antibodies. We found that no CD3+ cells underwent autophagy (Fig 4A), most autophagic cells colocalized with thymic epithelial cells (Fig 4C), and only some cells that underwent autophagy colocalized with CD14+ cells (Fig 4B).


Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Infection Induced Apoptosis and Autophagy in Thymi of Infected Piglets.

Wang G, Yu Y, Tu Y, Tong J, Liu Y, Zhang C, Chang Y, Wang S, Jiang C, Zhou EM, Cai X - PLoS ONE (2015)

Colocalization of CD3+ cells, CD14+ cells, thymic epithelial cells, and autophagic cells.CD3+ cells were stained with spectral red (SPRD)-conjugated mouse anti-pig CD3 antibodies, and autophagic cells were stained with anti-LC3 primary antibodies and anti-rabbit secondary antibodies conjugated to FITC, no CD3+ cells underwent autophagy (A); CD14+ cells were stained with FITC-conjugated mouse anti-pig CD14 antibodies and autophagic cells were stained with anti-LC3 primary antibodies and TRITC-conjugated goat anti-mouse antibodies, some CD14+ cells underwent autophagy (arrows) (B). Thymic epithelial cells were stained with mouse anti-pan-cytokeratin (P-CK) antibodies and FITC-conjugated goat anti-mouse antibodies, and autophagic cells were stained with anti-LC3 primary antibodies and TRITC-conjugated goat anti-mouse antibodies, most autophagic cells colocalized with thymic epithelial cells (arrows) (C). Nuclei were stained with DAPI.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4457848&req=5

pone.0128292.g004: Colocalization of CD3+ cells, CD14+ cells, thymic epithelial cells, and autophagic cells.CD3+ cells were stained with spectral red (SPRD)-conjugated mouse anti-pig CD3 antibodies, and autophagic cells were stained with anti-LC3 primary antibodies and anti-rabbit secondary antibodies conjugated to FITC, no CD3+ cells underwent autophagy (A); CD14+ cells were stained with FITC-conjugated mouse anti-pig CD14 antibodies and autophagic cells were stained with anti-LC3 primary antibodies and TRITC-conjugated goat anti-mouse antibodies, some CD14+ cells underwent autophagy (arrows) (B). Thymic epithelial cells were stained with mouse anti-pan-cytokeratin (P-CK) antibodies and FITC-conjugated goat anti-mouse antibodies, and autophagic cells were stained with anti-LC3 primary antibodies and TRITC-conjugated goat anti-mouse antibodies, most autophagic cells colocalized with thymic epithelial cells (arrows) (C). Nuclei were stained with DAPI.
Mentions: Previously, we characterized HuN4-infected cells, which were CD14+ cells, and apoptotic cells, which were mainly CD3+ cells [21]. Here, to characterize the types of thymic cells undergoing autophagy, CD14+ cells were also stained with FITC-conjugated mouse anti-pig CD14 antibodies, CD3+ cells were stained with spectral red (SPRD)-conjugated mouse anti-pig CD3 antibodies, and thymic epithelial cells were stained with mouse anti-pan-cytokeratin (P-CK) antibodies and FITC-conjugated goat anti-mouse antibodies. LC3 was strained using both anti-LC3 polyclonal antibody and FITC/TRITC-conjugated goat anti-rabbit antibodies. We found that no CD3+ cells underwent autophagy (Fig 4A), most autophagic cells colocalized with thymic epithelial cells (Fig 4C), and only some cells that underwent autophagy colocalized with CD14+ cells (Fig 4B).

Bottom Line: These findings demonstrated that HP-PRRSV induces apoptosis in bystander cells, and induces autophagy in both infected and bystander cells in the thymus of infected piglets.Herein, we first present new data on the thymic lesions induced by HP-PRRSV, and show that apoptosis and autophagy are key mechanisms involved in cell survival and determinants of the severity of thymic atrophy in infected piglets.Finally, future studies of the mechanism underlying immune responses are proposed based on our current understanding of PRRSV-host interactions.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, 150001, PR China.

ABSTRACT
Previously, we demonstrated that the highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) HuN4 strain causes obvious thymic atrophy and thymocytes apoptosis in infected piglets after birth, which is more severe than that induced by classical PRRSV. In this study, we investigated apoptosis and autophagy in the thymus of piglets infected with the HP-PRRSV HuN4 strain, and found that both apoptosis and autophagy occurred in the thymus of piglets infected with HP-PRRSV. In addition to a few virus-infected cells, CD14+ cells, the main autophagic cells in the thymus were thymic epithelial cells. These findings demonstrated that HP-PRRSV induces apoptosis in bystander cells, and induces autophagy in both infected and bystander cells in the thymus of infected piglets. Herein, we first present new data on the thymic lesions induced by HP-PRRSV, and show that apoptosis and autophagy are key mechanisms involved in cell survival and determinants of the severity of thymic atrophy in infected piglets. Finally, future studies of the mechanism underlying immune responses are proposed based on our current understanding of PRRSV-host interactions.

No MeSH data available.


Related in: MedlinePlus