Imperial College London
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ProfessorJ SimonKroll

Faculty of Medicine, Department of Infectious Disease

Emeritus Professor,Paediatrics&Molecular Infectious Diseases
 
 
 
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Contact

 

+44 (0)20 7594 3695s.kroll

 
 
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Assistant

 

Dr Robert Boyle +44 (0)20 7594 3990

 
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Location

 

245Wright Fleming WingSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Shaw:2021:10.1186/s12866-021-02285-0,
author = {Shaw, A and Sim, K and Rose, G and Wooldridge, D and Li, M-S and Misra, R and Gharbia, S and Kroll, JS},
doi = {10.1186/s12866-021-02285-0},
journal = {BMC Microbiology},
pages = {1--11},
title = {Premature neonatal gut microbial community patterns supporting an epithelial TLR-mediated pathway for necrotizing enterocolitis},
url = {http://dx.doi.org/10.1186/s12866-021-02285-0},
volume = {21},
year = {2021}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Background: Necrotising enterocolitis (NEC) is a devastating bowel disease, primarilyaffecting premature infants, with a poorly understood aetiology. Prior studies havefound associations in different cases with an overabundance of particular elements ofthe faecal microbiota (in particular Enterobacteriaceae or Clostridium perfringens ),but there has been no explanation for the different results found in different cohorts.Immunological studies have indicated that stimulation of the TLR4 receptor is involvedin development of NEC, with TLR4 signalling being antagonised by the activated TLR9receptor. We speculated that differential stimulation of these two components of thesignalling pathway by different microbiota might explain the dichotomous findings ofmicrobiota-centered NEC studies.  Here we used shotgun metagenomic sequencingand qPCR to characterise the faecal microbiota community of infants prior to NEConset and in a set of matched controls. Bayesian regression was used to segregatecases from control samples using both microbial and clinical data.Results: We found that the infants suffering from NEC fell into two groups based ontheir microbiota; one with low levels of CpG DNA in bacterial genomes and the otherwith high abundances of organisms expressing LPS. The identification of thesecharacteristic communities was reproduced using an external metagenomic validationdataset. We propose that these two patterns represent the stimulation of a commonpathway at extremes; the LPS-enriched microbiome suggesting overstimulation ofTLR4, whilst a microbial community with low levels of CpG DNA suggests reduction ofthe counterbalance to TLR4 overstimulation.Conclusions: The identified microbial community patterns support the concept of NECresulting from TLR-mediated pathways. Identification of these signals suggestscharacteristics of the gastrointestinal microbial community to be avoided to preventNEC. Potential pre- or pro-biotic treatments may be designed to optimise TLRsig
AU  - Shaw,A
AU  - Sim,K
AU  - Rose,G
AU  - Wooldridge,D
AU  - Li,M-S
AU  - Misra,R
AU  - Gharbia,S
AU  - Kroll,JS
DO  - 10.1186/s12866-021-02285-0
EP  - 11
PY  - 2021///
SN  - 1471-2180
SP  - 1
TI  - Premature neonatal gut microbial community patterns supporting an epithelial TLR-mediated pathway for necrotizing enterocolitis
T2  - BMC Microbiology
UR  - http://dx.doi.org/10.1186/s12866-021-02285-0
UR  - https://bmcmicrobiol.biomedcentral.com/articles/10.1186/s12866-021-02285-0
UR  - http://hdl.handle.net/10044/1/90915
VL  - 21
ER  -
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