Antibacterial and Anti-Inflammatory Effects of Lactobacillus reuteri in its Biofilm State Contribute to its Beneficial Effects in a Rat Model of Experimental Necrotizing Enterocolitis
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Read the article on jpedsurg.org ↗Article · Sep 2021 · 1 min read
In brief
In brief
Study demonstrates that Lactobacillus reuteri in biofilm form significantly reduces necrotizing enterocolitis incidence in premature rat models (67% to 18%), requiring both antimicrobial reuterin and anti-inflammatory histamine properties for efficacy. Findings suggest NEC pathogenesis involves both infectious and inflammatory mechanisms.
Written by the GCMD Library team from the article.
Introduction
: Necrotizing enterocolitis (NEC) remains a significant surgical emergency in neonates. We have demonstrated the efficacy of Lactobacillus reuteri (Lr) in protecting against experimental NEC when administered as a biofilm by incubation with maltose loaded dextranomer microspheres. Lr possesses antimicrobial and anti-inflammatory properties. We developed mutant strains of Lr to examine the importance of its antimicrobial and anti-inflammatory properties in protecting the intestines from NEC.
Methods
: Premature rat pups were exposed to hypoxia/hypothermia/hypertonic feeds to induce NEC. To examine the importance of antimicrobial reuterin and anti-inflammatory histamine, pups received either native or mutant forms of Lr, in either its planktonic or biofilm states, prior to induction of NEC. Intestinal histology was examined upon sacrifice.
Results
: Compared to no treatment, administration of a single dose of Lr in its biofilm state significantly decreased the incidence of NEC (67% vs. 18%, p< 0.0001), whereas Lr in its planktonic state had no significant effect. Administration of reuterin-deficient or histamine-deficient forms of Lr, in either planktonic or biofilm states, resulted in significant loss of efficacy.
Conclusion
: Antimicrobial and anti-inflammatory effects of Lr contribute to its beneficial effects against NEC. This suggests that both infectious and inflammatory components contribute to the etiology of NEC.