A Mouse Model of Necrotizing Enterocolitis

Mihi, Belgacem; Lanik, Wyatt E.; Gong, Qing; Good, Misty

doi:10.1007/978-1-0716-1488-4_9

Cited by 8 publications

(5 citation statements)

References 17 publications

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“…Newborn mice have a relatively immature intestinal tract compared to humans, lacking intestinal crypts and Paneth cells at birth and developing their intestines postnatally (8,21). To adjust for this developmental difference, many rodent models of NEC need to be performed 1-2 weeks after birth (14,19,20,(25)(26)(27)(28). In addition, rodent models can pose size-related challenges that make certain types of imaging, vascular cannulation, and sequential blood sampling difficult.…”

Section: Open Access Edited Bymentioning

confidence: 99%

Paneth cell ontogeny in term and preterm ovine models

Bautista,

Cera,

Schoenauer

et al. 2024

Front. Vet. Sci.

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IntroductionPaneth cells are critically important to intestinal health, including protecting intestinal stem cells, shaping the intestinal microbiome, and regulating host immunity. Understanding Paneth cell biology in the immature intestine is often modeled in rodents with little information in larger mammals such as sheep. Previous studies have only established the distribution pattern of Paneth cells in healthy adult sheep. Our study aimed to examine the ontogeny, quantification, and localization of Paneth cells in fetal and newborn lambs at different gestational ages and with perinatal transient asphyxia. We hypothesized that ovine Paneth cell distribution at birth resembles the pattern seen in humans (highest concentrations in the ileum) and that ovine Paneth cell density is gestation-dependent.MethodsIntestinal samples were obtained from 126–127 (preterm, with and without perinatal transient asphyxia) and 140–141 (term) days gestation sheep. Samples were quantified per crypt in at least 100 crypts per animal and confirmed as Paneth cells through in immunohistochemistry.ResultsPaneth cells had significantly higher density in the ileum compared to the jejunum and were absent in the colon.DiscussionExposure to perinatal transient asphyxia acutely decreased Paneth cell numbers. These novel data support the possibility of utilizing ovine models for understanding Paneth cell biology in the fetus and neonate.

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Section: Open Access Edited Bymentioning

confidence: 99%

Paneth cell ontogeny in term and preterm ovine models

Bautista,

Cera,

Schoenauer

et al. 2024

Front. Vet. Sci.

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“…To elucidate the relevant pathological mechanism, a mouse model of hypoxic-ischemic intestinal injury was generated following the animal model establishment method considered closest to neonatal patients with NEC. 13 We aimed to analyze the roles of I-FABP protein/mRNA, IL-6, and intestinal mucosal barrier disruption in the pathogenesis of NEC. Consistency between the NEC mouse model and human data was verified through macroscopic observation of specimens and microscopic pathological analysis and comparison of laboratory indicators.…”

Section: Introductionmentioning

confidence: 99%

I-FABP protein/mRNA and IL-6 as biomarkers of intestinal barrier dysfunction in neonates with necrotizing enterocolitis and SPF BALB/c mouse models

Chen,

Yan,

Lin

et al. 2024

J Int Med Res

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Objective Neonatal necrotizing enterocolitis (NEC) is a serious intestinal inflammatory disease. We investigated intestinal fatty acid binding protein (I-FABP), I-FABP mRNA, and interleukin-6 (IL-6) as potential diagnostic biomarkers in NEC. Methods Forty mice were subjected to hypoxic-ischemic intestinal injury, and then serum I-FABP protein and mRNA levels were quantified. Ileal tissue pathological scores were determined by hematoxylin and eosin staining. I-FABP expression levels and translocation in these tissues were detected using western blotting and immunofluorescence, respectively. Samples from 30 human neonates with NEC and 30 healthy neonates had serum I-FABP protein/mRNA and IL-6 levels measured. Results The mouse ileal tissue pathological score and I-FABP levels, as well as serum I-FABP and I-FABP mRNA levels, were significantly higher in the model group than in the control group. Serum I-FABP, I-FABP mRNA, and IL-6 levels were significantly higher in human neonates with NEC than in the healthy group. Logistic regression and receiver operating curve analyses revealed that I-FABP protein/mRNA and IL-6 levels could be diagnostic biomarkers for NEC. Conclusions I-FABP protein/mRNA and IL-6 levels are useful biomarkers of intestinal ischemic injury in neonates with NEC. The combined detection of I-FABP protein/mRNA and IL-6 is recommended rather than using a single biomarker.

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“…Necrotizing enterocolitis (NEC) remains a leading cause of morbidity and mortality in premature infants, with mortality rates as high as 10%–50% ( 1 , 2 ). Clinically, NEC can rapidly progress from relatively mild feeding intolerance and abdominal distension to bowel ischemia and necrosis, fulminant septic shock, severe acidosis, multi-organ dysfunction, and death.…”

Section: Introductionmentioning

confidence: 99%

“…These models subjected mouse pups to some combination of formula feeds, hypoxia, hypothermia, LPS, and/or bacterial dysbiosis/colonization to induce NEC-like injuries ( 9 , 82 ). More recently, Mihi et al (2021) described a version of these adapted HHF models that removes hypothermia but includes hypoxic stress, formula supplemented with LPS, and enteric bacteria derived from an infant who died from NEC totalis, the most severe form of NEC (“NECteria”) ( 1 ). In addition, early mouse models of NEC initially attempted to deliver pups via cesarean section immediately before term to prevent exposure to maternal milk like in the rat models ( 9 ).…”

Section: Introductionmentioning

confidence: 99%

State-of-the-art review and update of in vivo models of necrotizing enterocolitis

et al. 2023

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NEC remains one of the most common causes of mortality and morbidity in preterm infants. Animal models of necrotizing enterocolitis (NEC) have been crucial in improving our understanding of this devastating disease and identifying biochemical pathways with therapeutic potential. The pathogenesis of NEC remains incompletely understood, with no specific entity that unifies all infants that develop NEC. Therefore, investigators rely on animal models to manipulate variables and provide a means to test interventions, making them valuable tools to enhance our understanding and prevent and treat NEC. The advancements in molecular analytic tools, genetic manipulation, and imaging modalities and the emergence of scientific collaborations have given rise to unique perspectives and disease correlates, creating novel pathways of investigation. A critical review and understanding of the current phenotypic considerations of the highly relevant animal models of NEC are crucial to developing novel therapeutic and preventative strategies for NEC.

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A Mouse Model of Necrotizing Enterocolitis

Cited by 8 publications

References 17 publications

Paneth cell ontogeny in term and preterm ovine models

Paneth cell ontogeny in term and preterm ovine models

I-FABP protein/mRNA and IL-6 as biomarkers of intestinal barrier dysfunction in neonates with necrotizing enterocolitis and SPF BALB/c mouse models

State-of-the-art review and update of in vivo models of necrotizing enterocolitis

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