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γ-干扰素诱导的老年大鼠巨噬细胞中超氧阴离子和肿瘤坏死因子-α分泌的启动作用下降。

Interferon-gamma-induced priming for secretion of superoxide anion and tumor necrosis factor-alpha declines in macrophages from aged rats.

作者信息

Davila D R, Edwards C K, Arkins S, Simon J, Kelley K W

机构信息

Department of Animal Sciences, University of Illinois, Urbana 61801.

出版信息

FASEB J. 1990 Aug;4(11):2906-11. doi: 10.1096/fasebj.4.11.2165948.

DOI:10.1096/fasebj.4.11.2165948
PMID:2165948
Abstract

Macrophage responses to recombinant IFN-gamma decline during aging, as measured by two criteria of macrophage activation, O2- and TNF-alpha secretion. The production of O2- by macrophages in response to opsonized-zymosan and recombinant rat IFN-gamma is 75% lower in 23-month-old rats than in 3-month-old rats. Furthermore, the secretion of TNF-alpha in response to IFN-gamma and LPS is almost absent in macrophages from aged rats. Production of both O2- and TNF-alpha by resident peritoneal macrophages from specific pathogen-free aged rats in response to priming and triggering stimuli was partially or fully restored by implantation of syngeneic pituitary grafts from young rats. These data demonstrate that macrophages from aged rats are defective in their response to a priming signal induced by IFN-gamma, and they suggest that impaired macrophage responses during aging may be reversible.

摘要

通过巨噬细胞激活的两个指标——超氧阴离子(O2-)和肿瘤坏死因子-α(TNF-α)分泌来衡量,巨噬细胞对重组干扰素-γ(IFN-γ)的反应在衰老过程中会下降。在23月龄大鼠中,巨噬细胞在响应调理酵母聚糖和重组大鼠IFN-γ时产生的O2-比3月龄大鼠低75%。此外,老年大鼠巨噬细胞对IFN-γ和脂多糖(LPS)的反应几乎不分泌TNF-α。来自无特定病原体老年大鼠的驻留腹膜巨噬细胞在响应启动和触发刺激时产生的O2-和TNF-α,通过植入来自年轻大鼠的同基因垂体移植物部分或完全恢复。这些数据表明,老年大鼠的巨噬细胞对IFN-γ诱导的启动信号反应存在缺陷,并且表明衰老过程中受损的巨噬细胞反应可能是可逆的。

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