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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