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Updated: Sep 30, 2025
A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis
Published on: November 30, 2021
Bifidobacterium longum Subspecies infantis Strain EVC001 Decreases Neonatal Murine Necrotizing Enterocolitis
Shiloh R Lueschow1, Timothy J Boly2, Steven A Frese3
1Department of Microbiology and Immunology, University of Iowa, Iowa City, IA 52242, USA.
Insights
Necrotizing enterocolitis (NEC) prevention may be possible with the probiotic *B. infantis* EVC001. This study found EVC001 reduced NEC in mice by restoring gut health and improving the intestinal barrier.
Area of Science:
- Microbiology
- Neonatal Research
- Gastroenterology
Background:
- Necrotizing enterocolitis (NEC) is a severe intestinal disease in preterm infants with high mortality and limited treatment options.
- Current research focuses on prevention, particularly exploring the role of probiotics in modulating the infant gut microbiome.
- Preterm infants often exhibit dysbiosis and inflammation, increasing NEC risk.
Purpose of the Study:
- To investigate the efficacy of *B. infantis* EVC001 in preventing experimental necrotizing enterocolitis (NEC).
- To determine if EVC001 modulates inflammatory responses and restores epithelial barrier function in NEC models.
- To assess the impact of EVC001 on the gut microbiome in the context of NEC.
Main Methods:
- Experimental NEC was induced in P14-16 C57Bl/6 mice using Paneth cell disruption with bacterial dysbiosis or formula feeding.
- Mice were gavaged with *B. infantis* EVC001 or a control.
- Analysis included serum cytokine levels, intestinal tissue examination for injury, and microbiome profiling.
Main Results:
- EVC001 significantly decreased NEC in a bacterial dysbiosis-dependent model.
- In the formula-feeding NEC model, no significant difference in injury was observed, but serum cytokine levels showed trending differences.
- EVC001 enhanced wound closure in intestinal epithelial monolayers, indicating improved barrier function.
Conclusions:
- *B. infantis* EVC001 demonstrates potential in preventing experimental NEC, particularly in models involving bacterial dysbiosis.
- The probiotic exhibits anti-inflammatory properties and promotes epithelial barrier restoration.
- Further research is warranted to elucidate the mechanisms and clinical applicability of EVC001 for NEC prevention in preterm infants.
Abstract:
Necrotizing enterocolitis (NEC) is a disease mainly of preterm infants with a 30-50% mortality rate and long-term morbidities for survivors. Treatment strategies are limited and have not improved in decades, prompting research into prevention strategies, particularly with probiotics. Recent work with the probiotic B. infantis EVC001 suggests that this organism may generate a more appropriate microbiome for preterm infants who generally have inappropriate gut colonization and inflammation, both risk factors for NEC. Experimental NEC involving Paneth cell disruption in combination with bacterial dysbiosis or formula feeding was induced in P14-16 C57Bl/6 mice with or without gavaged B. infantis. Following completion of the model, serum, small intestinal tissue, the cecum, and colon were harvested to examine inflammatory cytokines, injury, and the microbiome, respectively. EVC001 treatment significantly decreased NEC in a bacterial dysbiosis dependent model, but this decrease was model-dependent. In the NEC model dependent on formula feeding, no difference in injury was observed, but trending to significant differences was observed in serum cytokines. EVC001 also improved wound closure at six and twelve hours compared to the sham control in intestinal epithelial monolayers. These findings suggest that B. infantis EVC001 can prevent experimental NEC through anti-inflammatory and epithelial barrier restoration properties.
