Proinflammatory and Th1 cytokine alterations following ultraviolet radiation enhancement of disease due to influenza infection in mice.
Proinflammatory and Th1 cytokine alterations following ultraviolet radiation enhancement of disease due to influenza infection in mice.
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紫外线辐射增强小鼠流感感染导致的疾病后，促炎细胞因子和 Th1 细胞因子发生变化。
作者：
L. Ryan;Lisa R Copeland;M. Daniels;Elisabeth R. Costa;M. Selgrade
啮齿动物暴露于免疫抑制剂如臭氧、二恶英或紫外线辐射（UVR）导致流感病毒感染后发病率和死亡率增加。然而，这些不良反应与抑制病毒特异性免疫反应无关。我们的实验室表明，紫外线辐射增加了发病率，死亡率和发病机制的流感病毒，而不影响保护性免疫的病毒，衡量抵抗再感染，这表明紫外线辐射和其他免疫抑制污染物，如二恶英和臭氧可能会加剧早期反应，有助于原发性病毒感染的发病机制。在本研究中，我们研究了紫外线增强的死亡率的机制，在没有对病毒特异性免疫的影响，并测试了假设，即细胞因子水平的调制与死亡和体重减轻增加。将BALB/c小鼠暴露于8.2 kJ/m2 UVR，3天后感染亚致死性流感病毒感染（小鼠适应性香港流感A/68，H（3）N（2）的LD（40））。在肺匀浆（LH）和支气管肺泡灌洗液（BAL）中测定炎性细胞、促炎细胞因子和辅助性T淋巴细胞（Th 1和Th 2）产生的细胞因子的流入。UVR预暴露减少流感诱导的淋巴细胞流入感染后5天，但没有改变巨噬细胞和中性粒细胞流入肺，或增加病毒滴度显着。尽管在感染前接受UVR暴露的小鼠中干扰素（IFN）-γ、总白细胞介素（IL）-12、IL-6和TNF-α发生了改变，但与UVR诱导的体重减轻增加和流感感染导致的死亡率增加没有明确的相关性。
Exposure of rodents to immunosuppressive agents such as ozone, dioxin, or ultraviolet radiation (UVR) leads to increased morbidity and mortality following influenza virus infection. However, these adverse effects are not related to the suppression of virus-specific immune responses. Our laboratory showed that UVR increased the morbidity, mortality, and pathogenesis of influenza virus without affecting protective immunity to the virus, as measured by resistance to reinfection, suggesting that UVR and other immunosuppressive pollutants such as dioxin and ozone may exacerbate early responses that contribute to the pathogenesis of a primary viral infection. In the present study, we examined the mechanism of UVR-enhanced mortality in the absence of effects on virus-specific immunity and tested the hypothesis that modulation of cytokine levels was associated with increased deaths and body weight loss. BALB/c mice were exposed to 8.2 kJ/m(2) UVR and were infected 3 days later with a sublethal influenza virus infection (LD(40) of mouse-adapted Hong Kong influenza A/68, H(3)N(2)). Influx of inflammatory cells, proinflammatory cytokines, and cytokines produced by T-helper lymphocytes (Th1 and Th2) were measured in lung homogenates (LH) as well as in bronchoalveolar lavage fluid (BAL). UVR preexposure decreased the influenza-induced lymphocytic influx 5 days after infection, but did not alter macrophage and neutrophil influx into the lung, or increase virus titers significantly. Although interferon (IFN)-gamma, total interleukin (IL)-12, IL-6, and TNF-alpha were altered in mice that received UVR exposure prior to infection, no clear association was made that correlated with the UVR-induced increase in body weight loss and mortality due to influenza infection.
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DOI：
10.1152/ajplung.2001.280.1.l69
发表时间：
2001-01-01
影响因子：
4.9
作者：
Suliman, HB;Ryan, LK;Folz, RJ
通讯作者：
Folz, RJ
IL-12 对紫外线辐射免疫抑制和抑制细胞诱导的影响。
DOI：
--
发表时间：
1995
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Schmitt,DA;Owen-Schaub,L;Ullrich,SE
通讯作者：
Ullrich,SE
影响因子：
56.9
作者：
Guttridge, DC;Mayo, MW;Baldwin, AS
通讯作者：
Baldwin, AS
αβ 和 γδT 细胞亚群在病毒免疫中的作用。
影响因子：
29.7
作者：
Doherty,PC;Allan,W;Eichelberger,M;Carding,SR
通讯作者：
Carding,SR
内毒素休克的内源性介质。
DOI：
--
发表时间：
1987
期刊：
Clinical research
影响因子：
--
作者：
Beutler,B;Cerami,A
通讯作者：
Cerami,A