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Upregulation of defensins in burn sheep small intestine.

作者信息

Poindexter Brian J, Klein Gordon L, Milner Stephen M, Bick Roger J

机构信息

Department of Pathology and Laboratory Medicine, University of Texas Medical School, Houston, USA.

出版信息

Eplasty. 2009 Dec 26;10:e6.

PMID:20076788
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2803769/
Abstract

OBJECTIVE

The aim of this study was to visualize and localize the sheep antimicrobials, beta-defensins 1, 2, and 3, (SBD-1, SBD-2, SBD-3), sheep neutrophil defensin alpha (SNP-1), and the cathelicidin LL-37 in sheep small intestine after burn injury, our hypothesis being that these compounds would be upregulated in an effort to overcome a compromised endothelial lining. Response to burn injury includes the release of proinflammatory cytokines and systemic immune suppression that, if untreated, can progress to multiple organ failure and death, so protective mechanisms have to be initiated and implemented.

METHODS

Tissue sections were probed with antibodies to the antimicrobials and then visualized with fluorescently labeled secondary antibodies and subjected to fluorescence deconvolution microscopy and image reconstruction.

RESULTS

In both the sham and burn samples, all the aforementioned antimicrobials were seen in each of the layers of small intestine, the highest concentration being localized to the epithelium. SBD-2, SBD-3, and SNP-1 were upregulated in both enterocytes and Paneth cells, while SNP-1 and LL-37 showed increases in both the inner circular and outer longitudinal muscle layers of the muscularis externa following burn injury. Each of the defensins, except SBD-1, was also seen in between the muscle layers of the externa and while burn caused slight increases of SBD-2, SBD-3, and SNP-1 in this location, LL-37 content was significantly decreased.

CONCLUSION

That while each of these human antimicrobials is present in multiple layers of sheep small intestine, SBD-2, SBD-3, SNP-1, and LL-37 are upregulated in the specific layers of the small intestine.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/70aabd335b0b/eplasty10e06_fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/40ffcac278ac/video_1_longitudinal_section_of_villi-thumb.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/6de83e6d58a8/video_2_microvilli-thumb.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/c70bdaee529a/video_3_x-section_of_crypt_high_power-thumb.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/32b626a1f9d4/video_4_x-section_of_crypts-thumb.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/f512ae454e9f/eplasty10e06_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/9e6be469a1ca/eplasty10e06_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/166bfd7d98d0/eplasty10e06_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/a61a486b0b6a/eplasty10e06_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/ea4b67475a06/eplasty10e06_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/bda8e5581893/eplasty10e06_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/20ac84ec384c/eplasty10e06_fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/70aabd335b0b/eplasty10e06_fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/40ffcac278ac/video_1_longitudinal_section_of_villi-thumb.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/6de83e6d58a8/video_2_microvilli-thumb.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/c70bdaee529a/video_3_x-section_of_crypt_high_power-thumb.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/32b626a1f9d4/video_4_x-section_of_crypts-thumb.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/f512ae454e9f/eplasty10e06_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/9e6be469a1ca/eplasty10e06_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/166bfd7d98d0/eplasty10e06_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/a61a486b0b6a/eplasty10e06_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/ea4b67475a06/eplasty10e06_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/bda8e5581893/eplasty10e06_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/20ac84ec384c/eplasty10e06_fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11f/2803769/70aabd335b0b/eplasty10e06_fig8.jpg

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本文引用的文献

1
Immunofluorescence deconvolution microscopy and image reconstruction of human defensins in normal and burned skin.
J Burns Wounds. 2005 Apr 25;4:e7.
2
Paneth cell alpha-defensin synthesis and function.潘氏细胞α-防御素的合成与功能。
Curr Top Microbiol Immunol. 2006;306:1-25. doi: 10.1007/3-540-29916-5_1.
3
Localization of antimicrobial peptides in normal and burned skin.抗菌肽在正常皮肤和烧伤皮肤中的定位。
Burns. 2006 Jun;32(4):402-7. doi: 10.1016/j.burns.2006.01.021. Epub 2006 Apr 18.
缺血再灌注后大鼠回肠和空肠中防御素的含量及定位变化。特定的肽,在特定的位置,执行特定的功能?
Eplasty. 2011 Feb 23;11:e8.
4
Expression of human beta defensin 2 in thermal injury.人β-防御素2在热损伤中的表达
Burns. 2004 Nov;30(7):649-54. doi: 10.1016/j.burns.2004.06.001.
5
Effects of cytokines and heat shock on defensin levels of cultured keratinocytes.细胞因子和热休克对培养的角质形成细胞防御素水平的影响。
Burns. 2004 Jun;30(4):329-33. doi: 10.1016/j.burns.2003.12.009.
6
Expression and regulation of antimicrobial peptides in the gastrointestinal tract.胃肠道中抗菌肽的表达与调控
J Leukoc Biol. 2004 Jan;75(1):49-58. doi: 10.1189/jlb.0503249. Epub 2003 Oct 2.
7
Inducibility of HBD-2 in acute burns and chronic conditions of the lung.
Burns. 2003 Sep;29(6):553-5. doi: 10.1016/s0305-4179(03)00145-1.
8
Macrophages and post-burn immune dysfunction.巨噬细胞与烧伤后免疫功能障碍
Burns. 2003 Feb;29(1):1-14. doi: 10.1016/s0305-4179(02)00187-0.
9
Cell differentiation is a key determinant of cathelicidin LL-37/human cationic antimicrobial protein 18 expression by human colon epithelium.细胞分化是人类结肠上皮细胞中cathelicidin LL-37/人类阳离子抗菌蛋白18表达的关键决定因素。
Infect Immun. 2002 Feb;70(2):953-63. doi: 10.1128/IAI.70.2.953-963.2002.
10
Human beta defensin is absent in burn blister fluid.人β-防御素在烧伤水疱液中不存在。
Burns. 2000 Dec;26(8):724-6. doi: 10.1016/s0305-4179(00)00052-8.