Related Experiment Video
Updated: Apr 11, 2026

08:14
Determining Membrane Protein Topology Using Fluorescence Protease Protection FPP
Published on: April 20, 2015
18.5K
Don't keep this endopeptidase on the DL.
Jaeden D Flury1, Drew J Schwartz2
1Department of Pediatrics, Division of Infectious Diseases, Washington University in St. Louis.
Cell Host & Microbe
|April 9, 2026
Summary
Delayed gut microbiome development in preterm infants increases the risk of late onset sepsis (LOS). A protective response involving NOD2 and gut-derived bacterial DL-endopeptidase was identified.
Area of Science:
- Microbiology
- Neonatal research
- Immunology
Background:
- Late onset sepsis (LOS) is a significant threat to preterm infants.
- Gut microbiome dysbiosis is increasingly recognized in neonatal intensive care.
Purpose of the Study:
- To investigate the link between gut microbiome development and LOS in preterm infants.
- To identify mechanisms of protection against LOS.
Main Methods:
- Analysis of gut microbiome composition in preterm infants.
- Investigation of immune responses involving NOD2 signaling.
Main Results:
- Delayed gut microbiome development identified as a risk factor for LOS.
- Gut-derived bacterial DL-endopeptidase proposed as a protective factor.
- NOD2 signaling implicated in the protective response.
Conclusions:
- Early-life gut microbiome maturation is crucial for preventing LOS in preterm neonates.
- NOD2-mediated pathways offer potential therapeutic targets for LOS prevention.
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