澳大利亚研究人员在人类呼吸道上皮细胞发现与呼吸道过敏性炎症有关的新蛋白aP2。aP2是脂肪细胞/巨噬细胞脂肪酸结合蛋白，已知与脂肪细胞聚集脂肪酸、糖尿病中阻抗胰岛素、动脉硬化有关。新研究发现，aP2在哮喘等呼吸道炎症扮演重要角色，此外与免疫系统和代谢系统间的联系有关。研究结果发表于7月份的电子版《临床调查杂志》上。
“卫生假说”（hygiene hypothesis）在医学领域研究哮喘潜在病因中一直占有统制地位。这一假说认为，儿童时代的感染以及环境因素如食物、空气污染等导致了哮喘的易感体质。
经过消毒处理的环境极可能是过敏、哮喘和Ⅰ型糖尿病、风湿病之类自身免疫性疾病患者激增的原因之一。此外，按照“卫生假说”理论，人们的免疫系统如果在早年生活中没有经受过疾病和肮脏的考验，人体的天然防御系统就会对花粉之类微小刺激物产生过度反应。Michael Rolph和其悉尼医学研究中心Garvan 研究所的同事首次证明：人类气管上皮细胞表达aP2蛋白，细胞因子白介素IL-4和 IL-13会刺激这类蛋白的大量表达。
这个发现令人惊奇，因为蛋白aP2以前一直被认为是脂肪细胞特异表达的。研究小组证明aP2缺陷的哮喘小鼠模型中 呼吸道炎症显著下降。
另外，在小鼠模型中白细胞、嗜曙红细胞等炎症分子渗入到 呼吸道需要依赖蛋白aP2的功能。这些强调了脂质在炎症反应中的重要性，有助于“炎症调节和新陈代谢调节路径具有重叠性的说法。最终，这项研究说明阻断蛋白aP2的功能，可能是治疗哮喘和其他类肺部炎症的新途径。
英文原文：
Asthma And Obesity Linked By Protein Called AP2
Adipocyte/macrophage fatty acid-binding protein aP2 (aP2), a protein which regulates allergic airway inflammation has been detected in human airway epithelial cells by scientists from the The Garvan Institute of Medical Research, Sydney, Australia. aP2 also regulates the uptake by lipid cells of fatty acids and is associated with insulin resistance and atherosclerosis.
In other words, aP2 not only helps bring about obesity, diabetes type 2, hardening of the arteries - it also plays a vital role in allergic respiratory diseases such as asthma. The scientists say this is the first discovery which sees a clear link between the immune and metabolic systems.
Michael Rolph, lead researcher, and team, found that mice lacking aP2 experience a significant reduction in airway inflammation in a model of asthma.
The scientists demonstrated for the first time that aP2 is present in human epithelial cells which line the tubes that carry air from the windpipe to the bronchi (lungs). They also showed that aP2 expression is dramatically increased when the epithelial cells are stimulated with interleukin-4 and -13. This was a surprise as scientists thought aP2 was a specific marker for fat cells only.
aP2 function in mice was directly linked to infiltration into the airways of leukocytes and eosinophils. Leukocytes and eosinophils are inflammatory molecules.
This discovery emphasizes the close link between the regulation of inflammation and metabolism.
The scientists say that a novel way of looking at asthma and other inflammatory lung disease treatments may be to block the function of aP2.
“The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation”
