TY - JOUR
T1 - Microarray analysis of mediastinal lymph node of pigs naturally affected by postweaning multisystemic wasting syndrome
AU - Fernandes, L. T.
AU - Tomás, A.
AU - Bensaid, A.
AU - Sibila, M.
AU - Sánchez, A.
AU - Segalés, J.
PY - 2012/5/1
Y1 - 2012/5/1
N2 - Postweaning multisystemic wasting syndrome (PMWS) is one of the pig diseases with major economic impact worldwide. Clinical, pathologic and some immunologic aspects of this disease are relatively well-known, but the molecular mechanisms underlying the pathogenic mechanisms of the disease are still poorly understood. The objective of the present study was to investigate the global transcriptome changes in the mediastinal lymph nodes from pigs naturally affected by PMWS, as well as healthy counterparts, using the Affymetrix Porcine Genechip ®. From 366 transcripts showing significant differential abundance in the PMWS group of pigs relative to healthy animals, 229 showed higher and 137 lower abundance. A relative increased abundance of mRNAs coded by a large set of genes involved in the inflammatory responses (e.g. cytokines, acute phase proteins, and respiratory burst) was observed in PMWS affected pigs. The Gpnmb and Lgals3 genes, which have antagonistic functions in regulation of inflammatory processes, showed high mRNA levels in diseased pigs. The complement system was altered by PMWS, notably by the lower levels of Cr1 mRNA, which might favour both complement deposition and secondary infections by impairing phagocytosis. Decreased mRNA abundance of several genes involved in lymphocyte activation/differentiation, such as Cd79b, Cd19, Cd21 and MybL1, and the high level of Vsig4 mRNA, which can compromise the activation of residing T-cells, pointed towards a defective adaptive immunity. This is the first study on gene expression in pigs naturally affected by PMWS. The present results allowed identifying potential mechanisms underlying the inflammation and lymphocyte depletion in lymphoid tissues by complement mediated damage and immunosuppression, which are key features of PMWS. © 2012 Elsevier B.V.
AB - Postweaning multisystemic wasting syndrome (PMWS) is one of the pig diseases with major economic impact worldwide. Clinical, pathologic and some immunologic aspects of this disease are relatively well-known, but the molecular mechanisms underlying the pathogenic mechanisms of the disease are still poorly understood. The objective of the present study was to investigate the global transcriptome changes in the mediastinal lymph nodes from pigs naturally affected by PMWS, as well as healthy counterparts, using the Affymetrix Porcine Genechip ®. From 366 transcripts showing significant differential abundance in the PMWS group of pigs relative to healthy animals, 229 showed higher and 137 lower abundance. A relative increased abundance of mRNAs coded by a large set of genes involved in the inflammatory responses (e.g. cytokines, acute phase proteins, and respiratory burst) was observed in PMWS affected pigs. The Gpnmb and Lgals3 genes, which have antagonistic functions in regulation of inflammatory processes, showed high mRNA levels in diseased pigs. The complement system was altered by PMWS, notably by the lower levels of Cr1 mRNA, which might favour both complement deposition and secondary infections by impairing phagocytosis. Decreased mRNA abundance of several genes involved in lymphocyte activation/differentiation, such as Cd79b, Cd19, Cd21 and MybL1, and the high level of Vsig4 mRNA, which can compromise the activation of residing T-cells, pointed towards a defective adaptive immunity. This is the first study on gene expression in pigs naturally affected by PMWS. The present results allowed identifying potential mechanisms underlying the inflammation and lymphocyte depletion in lymphoid tissues by complement mediated damage and immunosuppression, which are key features of PMWS. © 2012 Elsevier B.V.
KW - Gene expression
KW - Immune response
KW - Pig
KW - Porcine circovirus type 2
KW - Postweaning multisystemic wasting syndrome
U2 - https://doi.org/10.1016/j.virusres.2012.02.006
DO - https://doi.org/10.1016/j.virusres.2012.02.006
M3 - Article
VL - 165
SP - 134
EP - 142
JO - Virus Research
JF - Virus Research
SN - 0168-1702
ER -