Telles Tatiane M B B, de Oliveira Bruna M T, Lomba Luis A, Leite-Avalca Mariane G, Correia Diego, Zampronio Aleksander R
Department of Pharmacology, Federal University of Paraná, Curitiba, PR, Brazil.
Department of General Biology, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
Alcohol Clin Exp Res. 2017 Mar;41(3):507-515. doi: 10.1111/acer.13333. Epub 2017 Feb 13.
Ethanol (EtOH) exposure during different phases of life may increase the risk of infections and cause alterations in the central nervous system. The present study investigated the effects of binge-like EtOH exposure in adolescent rats on the febrile response that was induced by lipopolysaccharide (LPS) and interleukin-1β (IL-1β).
Male rats were exposed to EtOH from postnatal days 25 to 38 in a binge-like pattern. Fever was induced by LPS (5 and 50 μg/kg, intraperitoneally) and evaluated on postnatal days 51 and 63, or by IL-β (3 ng) and evaluated on postnatal day 51. Hematological parameters, the status of peritoneal macrophages, and plasma and cerebrospinal IL-1β levels were also evaluated on postnatal day 51.
EtOH exposure during adolescence did not alter normal body temperature. However, a significant reduction in the febrile response that was induced by LPS at both doses was observed on postnatal day 51. However, no changes in the febrile response were observed on postnatal day 63 in EtOH-exposed animals. The febrile response that was induced by intracerebroventricular IL-1β also significantly decreased in animals that received binge-like EtOH exposure during adolescence. Acute oral treatment with EtOH 24 h prior to LPS administration did not alter the febrile response that was induced by LPS. Binge-like EtOH exposure during adolescence did not alter hematological parameters or the number or viability of peritoneal macrophages. Binge-like EtOH exposure did not alter plasma IL-1β levels but reduced the cerebrospinal fluid levels of this cytokine.
These results suggest that binge-like EtOH exposure during adolescence causes changes in the central nervous system that can impair the febrile response that can be observed after the cessation of EtOH exposure. These changes were reversible and appeared to involve the LPS/IL-1β system.
在生命的不同阶段接触乙醇（EtOH）可能会增加感染风险并导致中枢神经系统发生改变。本研究调查了青春期大鼠暴饮样EtOH暴露对脂多糖（LPS）和白细胞介素-1β（IL-1β）诱导的发热反应的影响。
雄性大鼠在出生后第25天至38天以暴饮样模式接触EtOH。通过腹腔注射LPS（5和50μg/kg）诱导发热，并在出生后第51天和63天进行评估，或通过IL-β（3ng）诱导发热并在出生后第51天进行评估。还在出生后第51天评估血液学参数、腹腔巨噬细胞状态以及血浆和脑脊液中IL-1β水平。
青春期接触EtOH并未改变正常体温。然而，在出生后第51天观察到两种剂量的LPS诱导的发热反应均显著降低。但是，在出生后第63天，EtOH暴露动物的发热反应未观察到变化。青春期接受暴饮样EtOH暴露的动物，脑室内注射IL-1β诱导的发热反应也显著降低。在LPS给药前24小时急性口服EtOH并未改变LPS诱导的发热反应。青春期暴饮样EtOH暴露并未改变血液学参数或腹腔巨噬细胞的数量及活力。暴饮样EtOH暴露未改变血浆IL-1β水平，但降低了该细胞因子的脑脊液水平。
这些结果表明，青春期暴饮样EtOH暴露会导致中枢神经系统发生变化，从而损害在EtOH暴露停止后可观察到的发热反应。这些变化是可逆的，似乎涉及LPS/IL-1β系统。
