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Chemopreventive Metabolites Are Correlated with a Change in Intestinal Microbiota Measured in A-T Mice and Decreased Carcinogenesis.

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PubMed ID: 27073845

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Cheema AK, Maier I, Dowdy T, Wang Y, Singh R, Ruegger PM, Borneman J, Fornace AJ, Schiestl RH

PLoS One. 2016. doi: 10.1371/journal.pone.0151190

COMMENT: Ataxia telangiectasia (A-T) is a recessive genetic disorder of childhood that occurs 1/1000,000 individuals. Mutations in ATM gene are involved in A-T pathogenesis and there is a Atm-deficient mouse as model of the disease. ATM gene is a master controller of cell cycle checkpoint signaling pathways. More information about the Serine-protein kinase ATM protein encoded by ATM gene: http://www.uniprot.org/uniprot/Q13315

Approximately 30–40% of A-T patients develop neo-plasia during their life (40% non-Hodgkin’s lymphomas, ~20% acute lymphocytic leukemias, and 5% Hodgkin’s lymphomas). 

In this publication the authors use isogenic Atm-deficient and wild type mice with different controlled gut microbiomes to interrogate changes in the metabolic profiles of urine and feces. The two different microbiomes that they used were:

  • conventional microbiota (CM)
  • restricted microbiota (RM): few bacterial species dominated by unclassified Bacteroidetes and free of known pathogens

They show that the 2 different controlled microbiota tested appear to produce specific metabolic profiles in urine and feces. The metabolites 3-methylbutyrolactone, kyneurenic acid and 3-methyladenine known to be onco-protective were elevated in Atm-deficient and wild type mice with restricted intestinal microbiota (RM).

The onco-protective effect of restricted gut microbiota was detected for wild type mice and for Atm-KO mice.

Lactobacillus johnsonii was one of the indicator phylotypes more abundant in mice with restricted gut microbiome than in mice with conventional gut microbiome.

 

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Raquel Tobes