宿主对微生物分子的瞬时耐受性会带来许多感染性疾病，一般人们认为这种耐受性可以减少炎症引起的损伤，但实际上这种耐受性会改变宿主的防御功能。
Lu等人在9月11日的《细胞—宿主与微生物》（Cell Host & Microbe）杂志上报道了他们的发现：在缺乏脂酰基水解酶（AOAH）的小鼠体内，革兰氏阴性菌诱导的耐受性的恢复被大大推迟，AOAH具有部分去除细菌细胞壁脂多糖（LPS）的酰基作用。而野生型的小鼠在腹腔注射脂多糖或革兰阴性菌后可以在14天内恢复正常的反应，AOAH缺陷型小鼠则会大大降低前炎症反应，至少需要3周时间才能恢复注射脂多糖后的正常反应。与此相反，脂多糖引物-Aoah敲除的小鼠保持着的抗炎反应，这一点可从白细胞介素-10的血浆水平获知。脂多糖引物-Aoah敲除的小鼠经受了较长的耐受期，且对大肠杆菌高度敏感。
因此，灭活的脂多糖作为微生物的刺激免疫分子，对于恢复感染革兰阴性细菌动物的防御功能具有重要作用。（生物谷Bioon.com）
生物谷推荐原始出处：
Cell Host & Microbe，Vol 4, 293-302, 11 September 2008，Mingfang Lu, Robert S. Munford
Host Inactivation of Bacterial Lipopolysaccharide Prevents Prolonged Tolerance Following Gram-Negative Bacterial Infection
Mingfang Lu,1, Alan W. Varley,1 Shoichiro Ohta,2 John Hardwick,1 and Robert S. Munford1,
1 Infectious Disease Division, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-9113, USA
2 Department of Laboratory Medicine, Saga Medical School, 5-1-1 Nabeshima, Saga, Saga 849-8501, Japan
A transient state of tolerance to microbial molecules accompanies many infectious diseases. Such tolerance is thought to minimize inflammation-induced injury, but it may also alter host defenses. Here we report that recovery from the tolerant state induced by Gram-negative bacteria is greatly delayed in mice that lack acyloxyacyl hydrolase (AOAH), a lipase that partially deacylates the bacterial cell-wall lipopolysaccharide (LPS). Whereas wild-type mice regained normal responsiveness within 14 days after they received an intraperitoneal injection of LPS or Gram-negative bacteria, AOAH-deficient mice had greatly reduced proinflammatory responses to a second LPS injection for at least 3 weeks. In contrast, LPS-primed Aoah- knockout mice maintained an anti-inflammatory response, evident from their plasma levels of interleukin-10 (IL-10). LPS-primed Aoah-knockout mice experiencing prolonged tolerance were highly susceptible to virulent E. coli challenge. Inactivating LPS, an immunostimulatory microbial molecule, is thus important for restoring effective host defenses following Gram-negative bacterial infection in animals.
