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通过缺乏脂磷壁酸的嗜酸乳杆菌调节肠道免疫反应。

Modulating intestinal immune responses by lipoteichoic acid-deficient Lactobacillus acidophilus.

机构信息

Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA.

出版信息

Immunotherapy. 2012 Feb;4(2):151-61. doi: 10.2217/imt.11.163.

DOI:10.2217/imt.11.163
PMID:22339459
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3286340/
Abstract

AIM

To investigate the mechanism(s) by which the intestinal commensal microbe Lactobacillus acidophilus can affect host immunity, we studied the role of a component of the cell wall, lipoteichoic acid, in colitis.

MATERIALS & METHODS: Colitis was induced by the intraperitoneal injection of pathogenic CD4(+)CD25(-)CD45RB(hi) T cells into Rag1(-/-) mice. The parental strain, NCK56, or the lipoteichoic acid-deficient strain, NCK2025, was then administered orally. Fluorescent microscopy was employed to examine resulting cell populations and their cytokine production in the colon.

RESULTS

NCK2025 enhanced IL-10 production by dendritic cells and macrophages. Increased numbers of regulatory dendritic cells coincided with the induction of activated FoxP3(+) Tregs.

CONCLUSION

These results suggest that the oral administration of the genetically modified strain NCK2025 may be an effective immunotherapeutic approach that reprograms the immune response in colonic inflammatory conditions.

摘要

目的

为了研究肠道共生微生物嗜酸乳杆菌影响宿主免疫的机制，我们研究了细胞壁成分脂磷壁酸在结肠炎中的作用。

材料与方法

通过向 Rag1(-/-) 小鼠腹腔内注射致病性 CD4(+)CD25(-)CD45RB(hi)T 细胞来诱导结肠炎。然后，通过口服给予亲本菌株 NCK56 或脂磷壁酸缺陷菌株 NCK2025。采用荧光显微镜检查结肠中产生的细胞群及其细胞因子的产生。

结果

NCK2025 增强了树突状细胞和巨噬细胞中 IL-10 的产生。调节性树突状细胞数量的增加与激活的 FoxP3(+)Treg 的诱导同时发生。

结论

这些结果表明，口服给予基因修饰的 NCK2025 菌株可能是一种有效的免疫治疗方法，可以重塑结肠炎症条件下的免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/d9b871224d1e/nihms357056f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/271738a29c2a/nihms357056f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/cfc141c28709/nihms357056f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/d2d45b6a4492/nihms357056f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/9109ae610a7d/nihms357056f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/80a791d1e892/nihms357056f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/d9b871224d1e/nihms357056f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/271738a29c2a/nihms357056f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/cfc141c28709/nihms357056f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/d2d45b6a4492/nihms357056f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/9109ae610a7d/nihms357056f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/80a791d1e892/nihms357056f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b05b/3286340/d9b871224d1e/nihms357056f6.jpg

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