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野生型伤寒沙门氏菌Typhi 和减毒伤寒疫苗对体外肠道黏膜上皮的反应。

In vitro Intestinal Mucosal Epithelial Responses to Wild-Type Salmonella Typhi and Attenuated Typhoid Vaccines.

机构信息

Department of Pediatrics, Mucosal Biology Research Center, University of Maryland School of Medicine Baltimore, MD, USA.

出版信息

Front Immunol. 2013 Feb 12;4:17. doi: 10.3389/fimmu.2013.00017. eCollection 2013.

DOI:10.3389/fimmu.2013.00017
PMID:23408152
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3569575/
Abstract

Typhoid fever, caused by S. Typhi, is responsible for approximately 200,000 deaths per year worldwide. Little information is available regarding epithelium-bacterial interactions in S. Typhi infection. We have evaluated in vitro the effects of wild-type S. Typhi, the licensed Ty21a typhoid vaccine and the leading strains CVD 908-htrA and CVD 909 vaccine candidates on intestinal barrier function and immune response. Caco2 monolayers infected with wild-type S. Typhi exhibited alterations in the organization of tight junctions, increased paracellular permeability, and a rapid decrease in Trans-Epithelial Electrical Resistance as early as 4 h post-exposure. S. Typhi triggered the secretion of interleukin (IL)-8 and IL-6. Caco2 cells infected with the attenuated strains exhibited a milder pro-inflammatory response with minimal disruption of the barrier integrity. We conclude that wild-type S. Typhi causes marked transient alterations of the intestinal mucosa that are more pronounced than those observed with Ty21a or new generation attenuated typhoid vaccine candidates.

摘要

伤寒由伤寒沙门氏菌引起，每年导致全球约 20 万人死亡。关于伤寒沙门氏菌感染中上皮细胞与细菌的相互作用，目前相关信息有限。我们已在体外评估了野生型伤寒沙门氏菌、经许可的 Ty21a 伤寒疫苗以及主要的 CVD 908-htrA 和 CVD 909 疫苗候选株对肠道屏障功能和免疫应答的影响。感染野生型伤寒沙门氏菌的 Caco2 单层细胞表现出紧密连接结构紊乱、细胞旁通透性增加以及跨上皮电阻快速下降，这在暴露后 4 小时即可出现。伤寒沙门氏菌引发白细胞介素（IL）-8 和 IL-6 的分泌。减毒菌株感染 Caco2 细胞后，促炎反应较轻，对屏障完整性的破坏最小。综上，我们得出结论，野生型伤寒沙门氏菌会导致肠道黏膜发生明显的短暂改变，其严重程度超过 Ty21a 或新一代减毒伤寒疫苗候选株。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/197b/3569575/4dda369ec4d0/fimmu-04-00017-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/197b/3569575/cb6d911d8bb4/fimmu-04-00017-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/197b/3569575/13ca897e8cae/fimmu-04-00017-g009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/197b/3569575/107493d411c6/fimmu-04-00017-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/197b/3569575/3a3959c3efd0/fimmu-04-00017-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/197b/3569575/0ae24d981e97/fimmu-04-00017-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/197b/3569575/fb57510c8c44/fimmu-04-00017-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/197b/3569575/cc79327b915a/fimmu-04-00017-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/197b/3569575/cb6d911d8bb4/fimmu-04-00017-g008.jpg
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