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Comparison of two mice strains, A/J and C57BL/6, in caspase-1 activity and IL-1beta secretion of macrophage to Mycobacterium leprae infection.
Kang, Tae Jin; Lee, Geum Seon; Kim, Se Kon; Jin, Song Hou; Chae, Gue Tae.
Afiliación
  • Kang TJ; Institute of Chronic Disease, College of Pharmacy, Sahmyook University, 26-21 Kongnung 2-dong, Nowon-gu, Seoul 139-742, Republic of Korea. kangtj@syu.ac.kr
Mediators Inflamm ; 2010: 708713, 2010.
Article en En | MEDLINE | ID: mdl-20671924
A/J mice were found to have amino acid differences in Naip5, one of the NOD-like receptors (NLRs) involved in the cytosolic recognition of pathogen-associated molecular patterns and one of the adaptor proteins for caspase-1 activation. This defect was associated with a susceptibility to Legionella infection, suggesting an important role for Naip5 in the immune response also to other intracellular pathogens, such as Mycobacterium leprae. In this study, the immune responses of macrophages from A/J mice against M. leprae were compared to those of macrophages from C57BL/6 mice. Infection with M. leprae induced high levels of TNF-alpha production and NF-kappaB activation in A/J and C57BL/6 macrophages. Caspase-1 activation and IL-1beta secretion were also induced in both macrophages. However, macrophages from A/J mice exhibited reduced caspase-1 activation and IL-1beta secretion compared to C57BL/6 macrophages. These results suggest that NLR family proteins may have a role in the innate immune response to M. leprae.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Caspasa 1 / Interleucina-1beta / Sistema Inmunológico / Lepra / Macrófagos / Mycobacterium leprae Límite: Animals Idioma: En Revista: Mediators Inflamm Asunto de la revista: BIOQUIMICA / PATOLOGIA Año: 2010 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Caspasa 1 / Interleucina-1beta / Sistema Inmunológico / Lepra / Macrófagos / Mycobacterium leprae Límite: Animals Idioma: En Revista: Mediators Inflamm Asunto de la revista: BIOQUIMICA / PATOLOGIA Año: 2010 Tipo del documento: Article