一项最新研究显示，酩酊大醉带来的不仅是酒醒后的头痛，还有免疫系统功能下降，酒精对一些免疫功能的抑制会超过24小时。
美国科研人员在新一期英国《BMC免疫学》（BMC Immunology）杂志上报告说，他们检测了实验鼠在短时间内饮下大量酒精后其免疫系统所受影响。结果发现，酒精会抑制名为“TLR4”的蛋白质的作用，而这种蛋白质是许多有免疫作用的细胞因子的“信号员”，这些细胞因子被激活后会引发炎症等免疫反应，以帮助机体对抗细菌和病毒等。
实验显示，这些“信号员”在人醉酒后不能好好“站岗”，即便在醉酒24小时后，一些细胞因子仍然不能被激活。
研究人员因此提醒，大醉一场至少会带来24小时的免疫功能低下期，经常醉酒的人要警惕感染各种疾病的风险。（生物谷Bioon.com）
生物谷推荐原始出处：
BMC Immunology 2009, 10:49doi:10.1186/1471-2172-10-49
Ethanol inhibits LPS-induced signaling and modulates cytokine production in peritoneal macrophages in vivo in a model for binge drinking
Stephen B Pruett and Ruping Fan
Background
Previous reports indicate that ethanol, in a binge drinking model in mice, inhibits the production of pro-inflammatory cytokines in vivo. However, the inhibition of signaling through TLR4 has not been investigated in this experimental model in vivo. Considering evidence that signaling can be very different in vitro and in vivo, the present study was conducted to determine if effects of ethanol on TLR4 signaling reported for cells in culture or cells removed from ethanol treated mice and stimulated in culture also occur when ethanol treatment and TLR4 activation occur in vivo.
Results
Phosphorylated p38, ERK, and c-Jun (nuclear) were quantified with kits or by western blot using samples taken 15, 30, and 60 min after stimulation of peritoneal macrophages with lipopolysaccharide in vivo. Effects of ethanol were assessed by administering ethanol by gavage at 6 g/kg 30 min before administration of lipopolysaccharide (LPS). Cytokine concentrations in the samples of peritoneal lavage fluid and in serum were determined at 1, 2, and 6 hr after lipopolysaccharide administration. All of these data were used to measure the area under the concentration vs time curve, which provided an indication of the overall effects of ethanol in this system. Ethanol suppressed production of most pro-inflammatory cytokines to a similar degree as it inhibited key TLR4 signaling events. However, NF-kappaB (p65) translocation to the nucleus was not inhibited by ethanol. To determine if NF-kappaB composed of other subunits was inhibited, transgenic mice with a luciferase reporter were used. This revealed a reproducible inhibition of NF-kappaB activity, which is consistent with the observed inhibition of cytokines whose expression is known to be NF-kappaB dependent.
Conclusions
Overall, the effects of ethanol on signalling in vivo were similar to those reported for in vivo exposure to ethanol and/or lipopolysaccharide. However, inhibition of the activation of NF-kappaB was not detected as translocation of p65 to the nucleus but was detected using transgenic reporter mice. The observation that ethanol given 24 hr before dosing with LPS modulated production of some cytokines indicates a persistent effect which does not require continued presence of ethanol.
