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Aberrant TLR-mediated signal transduction in macrophages from aged mice
被引:0
作者:
Boehmer, E. D.
[1
,2
,4
]
Meehan, M. J.
[1
,2
]
Cutro, B. T.
[1
,2
]
Gomez, C. R.
[1
,2
,4
,5
]
Kovacs, E. J.
[1
,2
,3
,4
]
机构:
[1] Loyola Univ, Ctr Med, Dept Cell Biol Neurobiol & Anat, Maywood, IL 60153 USA
[2] Loyola Univ, Med Ctr, Burn & Shock Trauma Inst, Maywood, IL 60153 USA
[3] Loyola Univ, Med Ctr, Dept Surg, Maywood, IL 60153 USA
[4] Loyola Univ, Med Ctr, Immunol & Aging Program, Maywood, IL 60153 USA
[5] Univ Diego Portales, Fac Ciencias Salud, Santiago, Chile
来源:
PROCEEDINGS OF THE 6TH INTERNATIONAL CYTOKINE CONFERENCE
|
2006年
基金:
美国国家卫生研究院;
关键词:
D O I:
暂无
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Previously, we have reported that macrophages (M Phi s) from aged mice produce lower levels of cytokines than cells from young mice. Here, we examined Toll-like receptor (TLR) signaling pathways in murine M Phi s. LPS-and zymosan-stimulated production of TNF alpha and IL-6 was lower in M Phi s from aged mice when compared to young. These age-related changes were associated with lower activation of p38 MAPK and reduced expression of p38, but not MAPK-APK-2. These data suggest that decreased MAPK expression could be a mechanism responsible for the age-related deterioration of MFs function.
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页码:31 / +
页数:3
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