Acute cold/restraint stress inhibits host resistance to Listeria monocytogenes via β1-adrenergic receptors
Acute cold/restraint stress inhibits host resistance to Listeria monocytogenes via β1-adrenergic receptors
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DOI：
10.1016/s0889-1591(03)00026-6
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发表时间：
2003-04-01
影响因子：
15.1
通讯作者：
Lawrence, DA
中科院分区：
文献类型：
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作者：
Cao, L;Hudson, CA;Lawrence, DA
我们以前报道过，急性冷/约束应激（ACRS）显着抑制宿主对单核细胞增生李斯特菌（LM）在BALB/c小鼠和交感神经系统在这种抑制中起着重要作用。在这里，我们有进一步的。研究了肾上腺素能受体（ADR）亚型的参与。β-ADR拮抗剂普萘洛尔可显著增强ACRS小鼠的宿主抵抗力，而α-ADR拮抗剂酚妥拉明则无此作用。促炎细胞因子（IL-6、IL-1 β和TNF α）和IFN γ水平与所有小鼠组中的LM水平呈正相关。此外，β 1-ADR拮抗剂阿替洛尔而不是β 2-ADR拮抗剂ICI 118，551显著降低ACRS小鼠的LM负荷。此外，使用相同遗传背景的SCID小鼠（BALB/c）（无适应性免疫潜力）评估ACRS靶向的免疫应答。在SLID小鼠中未观察到ACRS诱导的宿主抗性抑制，普萘洛尔预处理未进一步改善宿主抗性，表明ACRS主要影响获得性免疫，这在先天免疫大于获得性免疫的小鼠中不太重要。总之，数据表明，ACRS抑制宿主对LM的耐药性是通过β 1-ADR刺激介导的，β 1-ADR刺激似乎直接或间接改变了T细胞的活化或随后参与适应性免疫的T细胞功能，从而抑制了整体宿主耐药性。有趣的是，如在SCID小鼠中观察到的，由于先天免疫增强和缺乏适应性免疫，ACRS不影响宿主抗性，这强调了先天免疫在防御细菌感染中的重要性。(C)2003 Elsevier Science（美国）。All rights reserved.
We previously reported that acute cold/restraint stress (ACRS) significantly inhibits host resistance to Listeria monocytogenes (LM) in BALB/c mice and that the sympathetic nervous system plays a major role in this inhibition. Here, we have further. investigated the involvement of adrenergic receptor (ADR) subtypes. beta-ADR antagonist propranolol, but not alpha-ADR antagonist phentolamine significantly enhanced host resistance of ACRS mice. Pro-inflammatory cytokine (IL-6, IL-1beta, and TNFalpha) and IFNgamma levels positively correlated with the LM levels in all groups of mice. Furthermore, beta1-ADR antagonist atenolol but not beta2-ADR antagonist ICI118,551 significantly decreased LM burden in ACRS mice. In addition, SCID mice on the same genetic background (BALB/c), which have no adaptive immune potential, were used to assess the immune responses targeted by ACRS. ACRS-induced suppression of host resistance was not observed in SLID mice, and propranolol pretreatment provided no further improvement of host resistance, indicating that ACRS mainly affects adaptive immunity, which is less critical in mice with greater innate than adaptive immunity. In summary, the data suggest that ACRS inhibition of host resistance to LM is mediated through beta1-ADR stimulation, which appears to directly or indirectly modify activation of T cells or subsequent T cell functions involved in adaptive immunity, thus inhibiting overall host resistance. Interestingly, with heightened innate immunity and the absence of adaptive immunity, as observed in the SCID mice, ACRS does not affect host resistance, which emphasizes the importance of innate immunity in defense against bacterial infection. (C) 2003 Elsevier Science (USA). All rights reserved.