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分枝杆菌感染可诱导小鼠嗜酸性粒细胞增多以及嗜酸性粒细胞产生α-防御素。

Mycobacterial infection induces eosinophilia and production of α-defensin by eosinophils in mice.

作者信息

Khatun Afia, Sakurai Masashi, Sakai Yusuke, Tachibana Masato, Ohara Naoya, Morimoto Masahiro

机构信息

Laboratory of Veterinary Pathology, Joint Faculty of Veterinary Medicine, Yamaguchi University, 1677-1, Yoshida, Yamaguchi 753-8515, Japan.

Department of Oral Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, 2-5-1 Shikata, Kita-ku, Okayama 700-8558, Japan.

出版信息

J Vet Med Sci. 2019 Jan 25;81(1):138-142. doi: 10.1292/jvms.18-0619. Epub 2018 Nov 23.

DOI:10.1292/jvms.18-0619
PMID:30473572
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6361637/
Abstract

It has been well known in humans that eosinophil infiltration into the site of inflammation and eosinophilia occur in mycobacterial infections. However, the role of eosinophils against the mycobacterium is unclear. We showed in previous study that in situ mouse eosinophils infiltrated into tissues produce α-defensin, an anti-bacterial peptide. We investigated in this study whether eosinophils reacting to mycobacteria produce α-defensin in mice and whether it can be used as a model. We showed that mycobacterial infection induced blood eosinophilia and infiltration of α-defensin producing eosinophils that to surround mycobacteria at the site of infection. These findings were usually seen during human mycobacterial infection. We established a good model to study host defense mechanism against mycobacteria through α-defensin via eosinophils.

摘要

在人类中,众所周知,嗜酸性粒细胞浸润到炎症部位以及嗜酸性粒细胞增多发生在分枝杆菌感染中。然而,嗜酸性粒细胞对抗分枝杆菌的作用尚不清楚。我们在先前的研究中表明,原位浸润到组织中的小鼠嗜酸性粒细胞会产生一种抗菌肽α-防御素。在本研究中,我们调查了对分枝杆菌产生反应的嗜酸性粒细胞是否会在小鼠中产生α-防御素,以及它是否可以用作模型。我们发现,分枝杆菌感染会诱导血液嗜酸性粒细胞增多以及产生α-防御素的嗜酸性粒细胞浸润,这些嗜酸性粒细胞会在感染部位包围分枝杆菌。这些发现通常在人类分枝杆菌感染期间可见。我们建立了一个很好的模型,用于通过嗜酸性粒细胞产生的α-防御素来研究宿主针对分枝杆菌的防御机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/2291547efcd4/jvms-81-138-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/c6a34f3fc7a8/jvms-81-138-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/6964f100cee1/jvms-81-138-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/453e6c62ae44/jvms-81-138-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/a7f92be4647d/jvms-81-138-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/933f41647a8d/jvms-81-138-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/2291547efcd4/jvms-81-138-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/c6a34f3fc7a8/jvms-81-138-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/6964f100cee1/jvms-81-138-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/453e6c62ae44/jvms-81-138-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/a7f92be4647d/jvms-81-138-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/933f41647a8d/jvms-81-138-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af21/6361637/2291547efcd4/jvms-81-138-g006.jpg

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