Trevejo-Nunez Giraldina, Chen Kong, Dufour Jason P, Bagby Gregory J, Horne William T, Nelson Steve, Kolls Jay K
Richard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Division of Comparative Pathology, Tulane National Primate Research Center, Covington, Louisiana, USA.
Infect Immun. 2015 May;83(5):2082-8. doi: 10.1128/IAI.02869-14. Epub 2015 Mar 9.
Acute ethanol intoxication suppresses the host immune responses against Streptococcus pneumoniae. As interleukin 17 (IL-17) is a critical cytokine in host defense against extracellular pathogens, including S. pneumoniae, we hypothesized that ethanol impairs mucosal immunity against this pathogen by disrupting IL-17 production or IL-17 receptor (IL-17R) signaling. A chronic ethanol feeding model in simian immunodeficiency virus (SIV)-infected rhesus macaques and acute ethanol intoxication in a murine model were used. Transcriptome analysis of bronchial brushes in the nonhuman primate model showed downregulation of the expression of IL-17-regulated chemokines in ethanol-fed animals, a finding also replicated in the murine model. Surprisingly, recombinant CXCL1 and CXCL5 but not IL-17 or IL-23 plus IL-1β rescued bacterial burden in the ethanol group to control levels. Taken together, the results of this study suggest that ethanol impairs IL-17-mediated chemokine production in the lung. Thus, exogenous luminal restoration of IL-17-related chemokines, CXCL1 and CXCL5, improves host defenses against S. pneumoniae.
急性乙醇中毒会抑制宿主针对肺炎链球菌的免疫反应。由于白细胞介素17(IL-17)是宿主抵御包括肺炎链球菌在内的细胞外病原体的关键细胞因子,我们推测乙醇通过破坏IL-17的产生或IL-17受体(IL-17R)信号传导来损害针对这种病原体的黏膜免疫。我们使用了感染猿猴免疫缺陷病毒(SIV)的恒河猴慢性乙醇喂养模型和小鼠急性乙醇中毒模型。非人灵长类动物模型中支气管刷的转录组分析显示,乙醇喂养的动物中IL-17调节的趋化因子表达下调,这一发现也在小鼠模型中得到了验证。令人惊讶的是,重组CXCL1和CXCL5而非IL-17或IL-23加IL-1β可将乙醇组的细菌载量恢复到对照水平。综上所述,本研究结果表明乙醇会损害肺部IL-17介导的趋化因子产生。因此,外源性恢复管腔内与IL-17相关的趋化因子CXCL1和CXCL5可改善宿主对肺炎链球菌的防御能力。