M. Gómez Cervantes, P. Luengo Batres, N. Huertos Soto, C. Rodríguez Bobada, MJ Fernández Aceñero, ´C Soto Beauregard
{"title":"Experimental necrotizing enterocolitis using oral lipopolysaccharide and protective role of breastmilk.","authors":"M. Gómez Cervantes, P. Luengo Batres, N. Huertos Soto, C. Rodríguez Bobada, MJ Fernández Aceñero, ´C Soto Beauregard","doi":"10.54847/cp.2024.02.14","DOIUrl":null,"url":null,"abstract":"INTRODUCTION\nNecrotizing enterocolitis (NEC) is a life-threatening condition that afflicts neonates. Breastfeeding has demonstrated to play a protective role against it. By administering lipopolysaccharides (LPS) orally in newborn rats (NBR), we have developed an experimental model to induce NEC-like gut damage. Our aim was to assess the macroscopic and microscopic appearance of the gut, to evaluate the presence of NEC and study the role of breast milk (BM).\n\n\nMATERIALS AND METHODS\nNBR were divided into 3 groups: Group A (control, n= 10) remained with the mother, group B (LPS, n= 25) was isolated after birth, gavage-fed with special rat formula and oral LPS, then submitted to stress (hypoxia after gavage) and group c (BM, n= 12) was breastfed once after birth, then isolated, and submitted to stress like group B. On day 4, NBR were sacrificed, and intestine was harvested and assessed.\n\n\nRESULTS\nIn the control group NEC was not present either macroscopically or histologically. Both groups submitted to stress (B and C) presented a global incidence of NEC of 73%. Most of group B developed histologic signs of NEC (85%) and group C showed a statistically lower incidence of NEC (50%, p= 0.04), playing the BM a protective role against NEC (OR= 0.19; 95% CI: 0.40-0.904).\n\n\nCONCLUSION\nOur model showed a significant incidence of NEC in NBR (73%) with the same protective role of BM as in newborn humans, achieving a reliable and reproducible experimental NEC model. This will allow us to investigate new potential therapeutic targets for a devastating disease that currently lacks treatment.","PeriodicalId":10316,"journal":{"name":"Cirugia pediatrica : organo oficial de la Sociedad Espanola de Cirugia Pediatrica","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cirugia pediatrica : organo oficial de la Sociedad Espanola de Cirugia Pediatrica","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.54847/cp.2024.02.14","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
INTRODUCTION
Necrotizing enterocolitis (NEC) is a life-threatening condition that afflicts neonates. Breastfeeding has demonstrated to play a protective role against it. By administering lipopolysaccharides (LPS) orally in newborn rats (NBR), we have developed an experimental model to induce NEC-like gut damage. Our aim was to assess the macroscopic and microscopic appearance of the gut, to evaluate the presence of NEC and study the role of breast milk (BM).
MATERIALS AND METHODS
NBR were divided into 3 groups: Group A (control, n= 10) remained with the mother, group B (LPS, n= 25) was isolated after birth, gavage-fed with special rat formula and oral LPS, then submitted to stress (hypoxia after gavage) and group c (BM, n= 12) was breastfed once after birth, then isolated, and submitted to stress like group B. On day 4, NBR were sacrificed, and intestine was harvested and assessed.
RESULTS
In the control group NEC was not present either macroscopically or histologically. Both groups submitted to stress (B and C) presented a global incidence of NEC of 73%. Most of group B developed histologic signs of NEC (85%) and group C showed a statistically lower incidence of NEC (50%, p= 0.04), playing the BM a protective role against NEC (OR= 0.19; 95% CI: 0.40-0.904).
CONCLUSION
Our model showed a significant incidence of NEC in NBR (73%) with the same protective role of BM as in newborn humans, achieving a reliable and reproducible experimental NEC model. This will allow us to investigate new potential therapeutic targets for a devastating disease that currently lacks treatment.
导言坏死性小肠结肠炎(NEC)是一种危及新生儿生命的疾病。事实证明,母乳喂养对NEC有保护作用。通过给新生大鼠(NBR)口服脂多糖(LPS),我们建立了一种诱发类似 NEC 肠道损伤的实验模型。我们的目的是评估肠道的宏观和微观外观,评估 NEC 的存在,并研究母乳(BM)的作用:A组(对照组,n= 10)与母亲呆在一起;B组(LPS,n= 25)出生后隔离,灌胃特殊大鼠配方奶粉和口服 LPS,然后接受应激(灌胃后缺氧);C组(BM,n= 12)出生后母乳喂养一次,然后隔离,与 B 组一样接受应激。接受应激的两组(B 组和 C 组)NEC 的总发生率均为 73%。结论我们的模型显示 NBR 中 NEC 的发病率很高(73%),而 BM 的保护作用与新生儿相同,从而建立了一个可靠且可重复的 NEC 实验模型。这将使我们能够研究新的潜在治疗靶点,以治疗这种目前缺乏治疗手段的毁灭性疾病。