Department of Medicine, Robert H Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Proc Natl Acad Sci U S A. 2012 Jun 26;109(26):10462-7. doi: 10.1073/pnas.1207230109. Epub 2012 Jun 11.
An imbalance of commensal bacteria and their gene products underlies mucosal and, in particular, gastrointestinal inflammation and a predisposition to cancer. Lactobacillus species have received considerable attention as examples of beneficial microbiota. We have reported previously that deletion of the phosphoglycerol transferase gene that is responsible for lipoteichoic acid (LTA) biosynthesis in Lactobacillus acidophilus (NCK2025) rendered this bacterium able to significantly protect mice against induced colitis when delivered orally. Here we report that oral treatment with LTA-deficient NCK2025 normalizes innate and adaptive pathogenic immune responses and causes regression of established colonic polyps. This study reveals the proinflammatory role of LTA and the ability of LTA-deficient L. acidophilus to regulate inflammation and protect against colonic polyposis in a unique mouse model.
共生菌及其基因产物的失衡是黏膜，特别是胃肠道炎症和癌症易感性的基础。乳杆菌属作为有益微生物群的例子受到了广泛关注。我们之前曾报道过，缺失负责嗜酸乳杆菌（NCK2025）中脂磷壁酸（LTA）生物合成的磷酸甘油转移酶基因，使这种细菌在口服给药时能够显著保护小鼠免受诱导性结肠炎。在这里，我们报告说，用缺乏 LTA 的 NCK2025 进行口服治疗可使固有和适应性致病性免疫反应正常化，并导致已建立的结肠息肉消退。这项研究揭示了 LTA 的促炎作用，以及缺乏 LTA 的嗜酸乳杆菌在独特的小鼠模型中调节炎症和预防结肠息肉形成的能力。
