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双歧双歧杆菌在坏死性小肠结肠炎大鼠模型中的抗菌肽和蛋白反应。

Bifidobacterium bifidum in a rat model of necrotizing enterocolitis: antimicrobial peptide and protein responses.

机构信息

Department of Pediatrics, University of California-Davis, Sacramento, California, USA.

出版信息

Pediatr Res. 2012 May;71(5):546-51. doi: 10.1038/pr.2012.11. Epub 2012 Feb 9.

DOI:10.1038/pr.2012.11
PMID:22322385
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3619207/
Abstract

INTRODUCTION

Necrotizing enterocolitis (NEC) is a devastating disease of premature infants. Probiotics decrease the risk of NEC in clinical and experimental studies. Antimicrobial peptides protect the gut against noxious microbes and shape the commensal microbiota, but their role in NEC remains unclear.

METHODS

To investigate the expression of antimicrobial peptides in experimental NEC and the impact of probiotics on their expression, premature rats were divided into three groups: dam fed (DF), hand fed with formula (FF), or hand fed with formula containing Bifidobacterium bifidum (FF + BIF). All groups were exposed to asphyxia and cold stress.

RESULTS

Like in human ontogeny, the rat pup has low expression of Paneth cell antimicrobials, which increases rapidly during normal development. The expression of lysozyme, secretory phospholipase A(2) (sPLA(2)), pancreatic-associated proteins 1 and 3 mRNA was elevated in the FF group with a high incidence of NEC, as compared with the DF and FF + BIF groups where the disease was attenuated.

DISCUSSION

We conclude that induction of antimicrobial peptides occurs in experimental NEC similar to that reported in human disease and is attenuated when disease is averted by probiotic B. bifidum. The induction of antimicrobial peptides is likely an adaptive mucosal response that is often not sufficient to prevent disease in the premature gut.

摘要

简介

坏死性小肠结肠炎(NEC)是早产儿的一种破坏性疾病。益生菌可降低临床和实验研究中 NEC 的风险。抗菌肽可保护肠道免受有害微生物的侵害,并塑造共生微生物群,但它们在 NEC 中的作用仍不清楚。

方法

为了研究实验性 NEC 中抗菌肽的表达以及益生菌对其表达的影响,将早产大鼠分为三组:母乳喂养组(DF)、人工喂养配方组(FF)或人工喂养含双歧杆菌组(FF+BIF)。所有组均暴露于窒息和冷应激中。

结果

与人类胚胎发育一样,幼鼠的潘氏细胞抗菌肽表达水平较低,在正常发育过程中迅速增加。与 DF 和 FF+BIF 组相比,FF 组中溶菌酶、分泌型磷脂酶 A2(sPLA2)、胰腺相关蛋白 1 和 3 mRNA 的表达升高,且 NEC 发病率较高,而在疾病减轻的 FF+BIF 组中则降低。

讨论

我们得出结论,实验性 NEC 中诱导抗菌肽的发生类似于人类疾病中报道的情况,并且当疾病被益生菌 B. bifidum 预防时则会减轻。抗菌肽的诱导可能是一种适应性黏膜反应,但在早产儿肠道中,这种反应通常不足以预防疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10e2/3619207/1e15a69babc8/nihms447418f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10e2/3619207/1253fc1dc6d4/nihms447418f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10e2/3619207/092a0f3fbd0f/nihms447418f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10e2/3619207/1e15a69babc8/nihms447418f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10e2/3619207/1253fc1dc6d4/nihms447418f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10e2/3619207/092a0f3fbd0f/nihms447418f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10e2/3619207/1e15a69babc8/nihms447418f3.jpg

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Paneth cell hyperplasia and metaplasia in necrotizing enterocolitis.坏死性小肠结肠炎中的潘氏细胞增生和化生。
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