一項(xiàng)最新研究顯示,，酩酊大醉帶來(lái)的不僅是酒醒后的頭痛,，還有免疫系統(tǒng)功能下降，酒精對(duì)一些免疫功能的抑制會(huì)超過(guò)24小時(shí),。
美國(guó)科研人員在新一期英國(guó)《BMC免疫學(xué)》（BMC Immunology）雜志上報(bào)告說(shuō),，他們檢測(cè)了實(shí)驗(yàn)鼠在短時(shí)間內(nèi)飲下大量酒精后其免疫系統(tǒng)所受影響,。結(jié)果發(fā)現(xiàn)，酒精會(huì)抑制名為“TLR4”的蛋白質(zhì)的作用,，而這種蛋白質(zhì)是許多有免疫作用的細(xì)胞因子的“信號(hào)員”,，這些細(xì)胞因子被激活后會(huì)引發(fā)炎癥等免疫反應(yīng)，以幫助機(jī)體對(duì)抗細(xì)菌和病毒等,。
實(shí)驗(yàn)顯示,，這些“信號(hào)員”在人醉酒后不能好好“站崗”，即便在醉酒24小時(shí)后,，一些細(xì)胞因子仍然不能被激活,。
研究人員因此提醒，大醉一場(chǎng)至少會(huì)帶來(lái)24小時(shí)的免疫功能低下期,，經(jīng)常醉酒的人要警惕感染各種疾病的風(fēng)險(xiǎn),。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
