Department of Infectious Diseases, St Jude Children's Research Hospital, Memphis, TN 38105-3678, USA.
Exp Biol Med (Maywood). 2010 Dec;235(12):1412-24. doi: 10.1258/ebm.2010.010227.
The world is now experiencing an epidemic of obesity. Although the effects of obesity on the development of metabolic and cardiovascular problems are well studied, much less is known about the impact of obesity on immune function and infectious disease. Studies in obese humans and with obese animal models have repeatedly demonstrated impaired immune function, including decreased cytokine production, decreased response to antigen/mitogen stimulation, reduced macrophage and dendritic cell function, and natural killer cell impairment. Recent studies have demonstrated that the impaired immune response in the obese host leads to increased susceptibility to infection with a number of different pathogens such as community-acquired tuberculosis, influenza, Mycobacterium tuberculosis, coxsackievirus, Helicobacter pylori and encephalomyocarditis virus. While no specific mechanism has been defined for the decreased immune response to infectious disease in the obese host, several obesity-associated changes such as excessive inflammation, altered adipokine signaling, metabolic changes and even epigenetic regulation could affect the immune response. This review will discuss what is currently known about the relationship between obesity and infectious disease.
目前全球正面临肥胖症的流行。虽然肥胖对代谢和心血管问题发展的影响已得到广泛研究,但人们对肥胖对免疫功能和传染病的影响知之甚少。对肥胖人群和肥胖动物模型的研究反复表明,免疫功能受损,包括细胞因子产生减少、对抗原/有丝分裂原刺激的反应减弱、巨噬细胞和树突状细胞功能降低以及自然杀伤细胞功能受损。最近的研究表明,肥胖宿主受损的免疫反应导致对多种不同病原体(如社区获得性肺结核、流感、结核分枝杆菌、柯萨奇病毒、幽门螺杆菌和脑炎心肌炎病毒)的易感性增加。虽然尚未为肥胖宿主对传染病的免疫反应降低确定特定的机制,但肥胖相关的一些变化,如过度炎症、脂肪因子信号改变、代谢变化甚至表观遗传调控,可能会影响免疫反应。本文将讨论目前已知的肥胖与传染病之间的关系。