T helper 1-type immunogenicity of Mycoplasma hyopneumoniae antigen on mouse spleen cells / 동물의과학연구지
Journal of Biomedical Research
; : 55-59, 2013.
Article
en Ko
| WPRIM
| ID: wpr-38429
Biblioteca responsable:
WPRO
ABSTRACT
Mycoplasma hyopneumoniae (M. hyopneumoniae) is one of the causative bacteria that can induce chronic enzootic pneumonia, resulting in low production in the swine industry. Potentiation of porcine reproductive and respiratory syndrome virus-induced pneumonia by M. hyopneumoniae has also been recognized. Although some available vaccines have been developed for prevention of M. hyopneumoniae infection, protective immunity is still poor. In this study, in order to provide valuable information on vaccine antigen, we investigated the immunogenicity of M. hyopneumoniae on mouse spleen cells. Concanavalin A (ConA) and lipopolysaccharide (LPS) were used for generation of activated T and B lymphocytes. M. hyopneumoniae made clusters of spleen cells and also affected the cellular activity and viability of spleen cells by alone or with mitogens. Of particular interest, it induced a significant increase in production of TNF-alpha in ConA-treated spleen cells, meaning T helper 1 response. In addition, cell size and mitochondrial membrane potential of M. hyopneumoniae-treated spleen cells were measured by flow cytometric analysis. M. hyopneumoniae did not affect the cell size by alone, whereas ConA or LPS profoundly increased the cell size. Taken together, M. hyopneumoniae significantly affect the cellular activity and cytokine production of spleen cells by alone or in a combination of ConA. This study provides valuable information for production of the vaccine against M. hyopneumoniae.
Palabras clave
Texto completo:
1
Índice:
WPRIM
Asunto principal:
Neumonía
/
Bazo
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Porcinos
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Bacterias
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Vacunas
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Linfocitos B
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Factor de Necrosis Tumoral alfa
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Concanavalina A
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Síndrome Respiratorio y de la Reproducción Porcina
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Mycoplasma hyopneumoniae
Límite:
Animals
Idioma:
Ko
Revista:
Journal of Biomedical Research
Año:
2013
Tipo del documento:
Article