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Published on: February 15, 2018
Neonatal small bowel epithelia: enhancing anti-bacterial defense with lactoferrin and Lactobacillus GG
Michael P Sherman1, Stephen H Bennett, Freda F Y Hwang
1School of Medicine, University of California, Davis, California, USA. mpsherman@ucdavis.edu
Insights
Early treatment with recombinant human lactoferrin (rhLF) and Lactobacillus GG (LGG) enhances gut defenses against Escherichia coli in infant rats. This combination may help prevent infections like necrotizing enterocolitis in preterm infants.
Area of Science:
- Gastroenterology
- Microbiology
- Neonatology
Background:
- Extremely preterm infants are vulnerable to small bowel infections.
- Enteroinvasive Escherichia coli poses a significant threat to this population.
Purpose of the Study:
- To investigate if early colonization with Lactobacillus GG (LGG) and recombinant human lactoferrin (rhLF) enhances gut defenses.
- To determine if rhLF promotes LGG growth in the immature small intestine.
Main Methods:
- Newborn rat pups were treated with LGG or rhLF + LGG.
- Gut colonization by LGG was quantified.
- Rats were infected with E. coli, and bacterial counts were measured in small bowel fluid and gut wall.
Main Results:
- LGG colonized the ileum more effectively than the jejunum.
- rhLF did not augment LGG colonization.
- Pre-treatment with rhLF and LGG significantly reduced E. coli growth in the small bowel.
Conclusions:
- Prophylactic rhLF and LGG enhance defenses against invasive E. coli in the developing small intestine.
- rhLF and LGG show potential as therapeutic agents to reduce necrotizing enterocolitis and sepsis in preterm infants.
Background And Aims:
Extremely preterm human infants have increased susceptibility to small bowel infection. We hypothesized that early colonization of the immature small intestine with Lactobacillus GG (LGG), and use of a recombinant lactoferrin (rhLF) to promote growth of LGG, would enhance gut defenses against enteroinvasive Escherichia coli.
Methods:
Newborn rat pups were treated with nothing, intra-gastric LGG, or rhLF + LGG on days 3 and 4 of life. Gut colonization by LGG was quantified in lavaged jejunal and ileal fluid and gut wall homogenates on day 5 of life. Separate studies used similarly treated litters of newborn rats that were infected late on day 4 of life with E. coli [10(12) CFU/kg]. Sixteen hours later, the numbers of E. coli were measured in small bowel fluid and gut wall homogenates.
Results:
Control pups initially had lactic acid bacteria colonize the bowel, but these bacteria were not LGG. Pups treated with LGG or rhLF + LGG had significantly higher numbers of LGG in the ileum versus jejunum. Contrary to our hypothesis, rhLF did not augment LGG colonization. After E. coli-related gut infection, planktonic [lavage fluid] and epithelia-adherent growth [gut wall homogenates] of E. coli in the small bowel were most effectively reduced by pre-treatment with rhLF and LGG (P < .05).
Conclusion:
Prophylactic therapy with recombinant human lactoferrin and the probiotic, Lactobacillus GG, act to enhance defenses against invasive E. coli in the nascent small intestine. We suggest that rhLF and LGG are therapeutic agents that may reduce necrotizing enterocolitis and gut-related sepsis in preterm human infants.
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