PNAS:经过改造的乳酸菌逆转了小鼠的结肠癌
导读 | 一项刊登在<em>PNAS</em>上的研究揭示了,食用经过遗传改造的嗜酸乳酸杆菌能重置小鼠的可能导致癌症的免疫应答,并缩小前癌结肠息肉。此前对益生肠道微生物嗜酸乳酸杆菌的研究已经表明,通过删除被称为脂磷壁酸(LTA)的细胞表面分子的基因,这种细菌可以减少导致小鼠结肠炎的炎症应答。
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为了研究脂磷壁酸(LTA)是否也是越来越被怀... |
一项刊登在<em>PNAS</em>上的研究揭示了,食用经过遗传改造的嗜酸乳酸杆菌能重置小鼠的可能导致癌症的免疫应答,并缩小前癌结肠息肉。此前对益生肠道微生物嗜酸乳酸杆菌的研究已经表明,通过删除被称为脂磷壁酸(LTA)的细胞表面分子的基因,这种细菌可以减少导致小鼠结肠炎的炎症应答。
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为了研究脂磷壁酸(LTA)是否也是越来越被怀疑促进了肿瘤的过度活跃的炎症应答的参与因素之一,Mansour Mohamadzadeh及其同事让有病理性炎症和前癌结肠息肉的小鼠口服了缺乏脂磷壁酸(LTA)的嗜酸乳酸杆菌。这组作者说,这种疗法重置了过度活跃的炎症应答,并且把试验对象的肠内环境恢复到了健康的平衡态,因此也就把肠粘膜解放出来,从而处理结肠息肉并使其退化。
这组作者说,除了表明消化道微生物群炎症参与免疫应答,这些发现还表明了嗜酸乳酸杆菌可能提供调控肠内免疫、逆转某些前癌状态并预防诸如结肠癌等炎症驱动的恶性肿瘤。
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<img src="http://www.bioon.com/biology/UploadFiles/201206/2012061210204642.jpg" alt="" width="113" height="149" border="0" />
<a title="" href="http://dx.doi.org/doi:10.1073/pnas.1207230109" target="_blank">doi:10.1073/pnas.1207230109</a>
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<br/><strong>Abating colon cancer polyposis by Lactobacillus acidophilus deficient in lipoteichoic acid</strong><br/>
Khashayarsha Khazaiea, Mojgan Zadeha,b, Mohammad W. Khana, Praveen Bereb, Fotini Gounaric, Kirsten Dennisa, Nichole R. Blatnera, Jennifer L. Owenb, Todd R. Klaenhammerd,1, and Mansour Mohamadzadeha,b,1
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.
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为了研究脂磷壁酸(LTA)是否也是越来越被怀疑促进了肿瘤的过度活跃的炎症应答的参与因素之一,Mansour Mohamadzadeh及其同事让有病理性炎症和前癌结肠息肉的小鼠口服了缺乏脂磷壁酸(LTA)的嗜酸乳酸杆菌。这组作者说,这种疗法重置了过度活跃的炎症应答,并且把试验对象的肠内环境恢复到了健康的平衡态,因此也就把肠粘膜解放出来,从而处理结肠息肉并使其退化。
这组作者说,除了表明消化道微生物群炎症参与免疫应答,这些发现还表明了嗜酸乳酸杆菌可能提供调控肠内免疫、逆转某些前癌状态并预防诸如结肠癌等炎症驱动的恶性肿瘤。
<div id="ztload">
<div>
<div>
<img src="http://www.bioon.com/biology/UploadFiles/201206/2012061210204642.jpg" alt="" width="113" height="149" border="0" />
<a title="" href="http://dx.doi.org/doi:10.1073/pnas.1207230109" target="_blank">doi:10.1073/pnas.1207230109</a>
PMC:
PMID:
</div>
<div>
<br/><strong>Abating colon cancer polyposis by Lactobacillus acidophilus deficient in lipoteichoic acid</strong><br/>
Khashayarsha Khazaiea, Mojgan Zadeha,b, Mohammad W. Khana, Praveen Bereb, Fotini Gounaric, Kirsten Dennisa, Nichole R. Blatnera, Jennifer L. Owenb, Todd R. Klaenhammerd,1, and Mansour Mohamadzadeha,b,1
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.
</div>
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