Suppression of host resistance to Listeria monocytogenes by acute cold/restraint stress:: lack of direct IL-6 involvement
Suppression of host resistance to Listeria monocytogenes by acute cold/restraint stress:: lack of direct IL-6 involvement
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DOI：
10.1016/s0165-5728(02)00371-5
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发表时间：
2002-12-01
影响因子：
3.3
通讯作者：
Lawrence, DA
中科院分区：
文献类型：
--
作者：
Cao, L;Lawrence, DA
我们进行了动力学研究，以评估急性冷/束缚应激(ACRS)对单核细胞增多性李斯特菌(Lm)一次和二次寄主抗性的影响。以BALB/c为背景，用IL-6基因敲除(KO)小鼠研究了IL-6的参与。ACRS显著升高血清皮质酮水平，提示ACRS激活了下丘脑-垂体-肾上腺(HPA)轴。ACRs在原发侵染期间显著抑制寄主对LM的抗性，但在继发侵染期间不显著。在初次感染期间，ACRS导致LM清除明显延迟，体重减轻，食物/水摄入量减少，促炎细胞因子(IL-6、IL-1β和TNFpha)和干扰素-γ水平升高。ACRS IL-6 KO小鼠表现出比IL-6 KO对照组更高的LM负荷，提示IL-6不是ACRS抵抗宿主所必需的。IL-1β和TNFα水平的升高可能弥补了IL-6的缺失，维持了ACRS诱导的损伤，因为感染ACRS的IL-6 KO小鼠的血清和脾IL-1β和TNFα水平显著高于各自的野生型对照小鼠，而对照IL-6 KO小鼠的IL-1β和TNFα水平并不显著高于各自的野生型对照。ACRs似乎抑制了与先天免疫和/或获得性免疫发展相关的IL-6独立机制，但这些反应无法调节更有效的二次免疫反应。(C)2002 Elsevier Science B.V.保留所有权利。
We conducted kinetic studies to evaluate the effects of acute cold/restraint stress (ACRS) on both primary and secondary host resistance to Listeria monocytogenes (LM). The involvement of IL-6 also was investigated using IL-6 knockout (KO) mice on the BALB/c background. ACRS dramatically increased the serum corticosterone levels, indicating that ACRS activated the hypothalamic-pituitary-adrenal (HPA) axis. ACRS significantly inhibited host resistance to LM during a primary but not a secondary LM infection. During the primary infection, ACRS caused a significant delay in clearance of LM, loss of body weight, reduced food/water intake, and elevated levels of pro-inflammatory cytokines (IL-6, IL-1beta, and TNFalpha) and IFN-gamma. ACRS IL-6 KO mice showed higher LM burdens than did IL-6 KO controls, suggesting that IL-6 is not required for the ACRS-impainnent of host resistance. Elevated levels of IL-1beta and TNFalpha may compensate for the absence of IL-6 and maintain the ACRS-induced impairment, in that the serum and splenic IL-1beta and TNFalpha levels were significantly higher in infected ACRS IL-6 KO mice, but not in control IL-6 KO mice, as compared to respective wild type controls. ACRS appears to inhibit IL-6 independent mechanisms associated with innate immunity and/or the development of adaptive immunity, but these reactions are unable to modulate the more efficient secondary immune responses. (C) 2002 Elsevier Science B.V All rights reserved.