PDF(Pubmed)
Abstract：
Air pollution is an urgent concern linked to numerous health problems in low- and middle-income countries, where 92% of air pollution-related deaths occur. Particulate matter 2.5 (PM2.5) is the most harmful component of air pollutants, increasing inflammation and changing gut microbiota, favoring obesity, type 2 diabetes, and Alzheimer\'s Disease (AD). PM2.5 contains lipopolysaccharides (LPS), which can activate the Toll-like receptor 4 (TLR4) signaling pathway. This pathway can lead to the release of pro-inflammatory markers, including interleukins, and suppressor of cytokine signaling-3 (SOCS3), which inhibits leptin action, a hormone that keeps the energy homeostasis. Leptin plays a role in preventing amyloid plaque deposition and hyperphosphorylation of tau-protein (p-tau), mechanisms involved in the neurodegeneration in AD. Approximately 50 million people worldwide are affected by dementia, with a significant proportion living in low-and middle-income countries. This number is expected to triple by 2050. This mini-review focuses on the potential impact of PM2.5 exposure on the TLR4 signaling pathway, its contribution to leptin resistance, and dysbiosis that exacerbates the link between obesity and AD.
摘要：
空气污染是与低收入和中等收入国家的许多健康问题有关的紧迫问题。其中92%的空气污染相关死亡发生。颗粒物2.5(PM2.5)是空气污染物中危害最大的成分,增加炎症和改变肠道微生物群，有利于肥胖，2型糖尿病,和阿尔茨海默病（AD）。PM2.5含有脂多糖（LPS），可以激活Toll样受体4(TLR4)信号通路。该途径可导致促炎标志物的释放，包括白细胞介素,和细胞因子信号转导抑制因子-3（SOCS3），抑制瘦素的作用，一种保持能量稳态的激素。瘦素在预防淀粉样斑块沉积和tau蛋白（p-tau）过度磷酸化中起作用，参与AD神经变性的机制。全世界约有5000万人患有痴呆症，很大一部分生活在中低收入国家。这个数字预计到2050年将增加两倍。这篇小型综述主要关注PM2.5暴露对TLR4信号通路的潜在影响，它对瘦素抗性的贡献，和生态失调加剧了肥胖和AD之间的联系。
