JLB:关注饮酒相关并存病
2015/4/3 医学论坛网

    

     酗酒会影响一个人的生活的方方面面,当然也包括皮肤问题,近日,一篇发表于国际杂志the Journal of Leukocyte Biology上的研究论文中,来自爱荷华大学的研究人员通过对小鼠进行研究揭示了长期饮酒如何中和肌体皮肤的保护性免疫防御力,同时研究者还揭示了如何通过特定的干预措施来改善机体皮肤的免疫防御能力,该研究或可帮助开发基于免疫的疗法来帮助长期饮酒的个体来抵御皮肤的感染。

     研究者Corey P. Parlet博士指出,临床研究中已经确定了酗酒和严重皮肤感染之间的关系,而在慢性酗酒模型中皮肤免疫力的缺失机制研究或为开发新型基于免疫的疗法来保护机体免于感染提供了新的线索。

     文章中研究者对小鼠制定了三种策略,包括含有20%酒精的水、水溶液及净水,在策略实施12周后,研究者评估了经金黄色葡萄球菌感染皮肤的小鼠机体的常规固体饮食量、感染预后情况及宿主防御力,结果显示,消耗酒精的小鼠的患病率增加,其机体体重降低、皮肤溃烂面增加及细菌感染负担增加;同时小鼠机体维持正常免疫细胞数量及特定感染位点的能力也下降了,尤其是中性白细胞的数量发生了明显的下降。

     白介素-17在正常情况下可以促进中性白细胞进入皮肤并且发挥作用,而研究者却发现白介素-17在消耗酒精的小鼠机体中数量明显下降了,通过恢复白介素-17的水平,小鼠皮肤的损伤水平就可以明显降低,而且细菌清除能力也得到了明显地改善。

     最后研究者John Wherry表示,和长期饮酒相关的并存病通常并不会得到个体的太多关注,然而其却会对个体的一生健康带来非常严重的影响,本文研究就可以帮助揭示如何通过控制白介素-17来改善机体的免疫力,进而帮助开发新型疗法来治疗个体酗酒相关的机体皮肤感染。

    

     doi:10.1189/JLB.4A0214-092R

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     Chronic ethanol feeding increases the severity of Staphylococcus aureus skin infections by altering local host defenses.

     Corey P. Parlet*, , Jeffrey S. Kavanaugh , Alexander R. Horswill and Annette J. Schlueter*, ,1

     Alcoholics are at increased risk of Staphylococcus aureus skin infection and serious sequelae, such as bacteremia and death. Despite the association between alcoholism and severe S. aureus skin infection, the impact of EtOH on anti-S. aureus cutaneous immunity has not been investigated in a model of chronic EtOH exposure. To test the hypothesis that EtOH enhances the severity of S. aureus skin infection, mice were fed EtOH for ≥12 weeks via the Meadows-Cook model of alcoholism and inoculated with S. aureus following epidermal abrasion. Evidence of exacerbated staphylococcal disease in EtOH-fed mice included: skin lesions that were larger and contained more organisms, greater weight loss, and increased bacterial dissemination. Infected EtOH-fed mice demonstrated poor maintenance and induction of PMN responses in skin and draining LNs, respectively. Additionally, altered PMN dynamics in the skin of these mice corresponded with reduced production of IL-23 and IL-1β by CD11b+ myeloid cells and IL-17 production by γδ T cells, with the latter defect occurring in the draining LNs as well. In addition, IL-17 restoration attenuated S. aureus-induced dermatopathology and improved bacterial clearance defects in EtOH-fed mice. Taken together, the findings show, in a novel model system, that the EtOH-induced increase in S. aureus-related injury/illness corresponds with defects in the IL-23/IL-17 inflammatory axis and poor PMN accumulation at the site of infection and draining LNs. These findings offer new information about the impact of EtOH on cutaneous host-defense pathways and provide a potential mechanism explaining why alcoholics are predisposed to S. aureus skin infection.

     来源:生物谷

    

    

    

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