Can Gut Microbiota and Lifestyle Help Us in the Handling of Anorexia Nervosa Patients?

Gut microbiota is composed of different microorganisms that play an important role in the host. New research shows that bidirectional communications happen between intestinal microbiota and the brain, which is known as the gut⁻brain axis. This communication is significant and could have a negative or positive effect depending on the state of the gut microbiota. Anorexia nervosa (AN) is a mental illness associated with metabolic, immunologic, biochemical, sensory abnormalities, and extremely low body weight. Different studies have shown a dysbiosis in patients with AN. Due to the gut⁻brain axis, it was observed that some of the symptoms could be improved in these patients by boosting their gut microbiota. This paper highlights some evidence connecting the role of microbiota in the AN onset and disease progress. Finally, a proposal is done to include the microbiota analysis as part of the recovery protocol used to treat AN patients. When conducting clinical studies of gut microbiota in AN patients, dysbiosis is expected to be found. Then the prescription of a personalized treatment rich in prebiotics and probiotics could be proposed to reverse the dysbiosis.

[Role of double strand DNA break repair for quinolone sensitivity in Escherichia coli: therapeutic implications]. / El papel de la reparación de roturas de doble cadena de ADN en Escherichia coli en la sensibilidad a quinolonas: implicaciones terapéuticas.

INTRODUCTION: Quinolones are one of the types of antibiotics with higher resistance rates in the last years. At molecular level, quinolones block type II topoisomerases producing double strand breaks (DSBs). These DSBs could play a double role, as inductors of the quinolone bactericidal effects but also as mediators of the resistance and tolerance mechanisms. MATERIAL AND METHODS: In this work we have studied the molecular pathways responsible for DSBs repair in the quinolone susceptibility: the stalled replication fork reversal (recombination-dependent) (RFR), the SOS response induction, the translesional DNA synthesis (TLS) and the nucleotide excision repair mechanisms (NER). For this reason, at the European University in Madrid, we analysed the minimal inhibitory concentration (MIC) to three different quinolones in Escherichia coli mutant strains coming from different type culture collections. RESULTS: recA, recBC, priA and lexA mutants showed a significant reduction on the MIC values for all quinolones tested. No significant changes were observed on mutant strains for TLS and NER. DISCUSSION: These data indicate that in the presence of quinolones, RFR mechanisms and the SOS response could be involved in the quinolone susceptibility.

El papel de la reparación de roturas de doble cadena de ADN en Escherichia coli en la sensibilidad a quinolonas: implicaciones terapéuticas / Role of double strand DNA break repair for quinolone sensitivity in Escherichia coli: therapeutic implications

Introducción. Las quinolonas son uno de los tipos de antibióticos cuyas tasas de resistencia se han visto incrementadas en los últimos años. A nivel molecular, bloquean a las topoisomerasas tipo II generando cortes de doble cadena (double strand breaks, DSBs) en el ADN. Se ha propuesto que estos DSBs podrían tener un doble papel, como mediadores de su efecto bactericida y también como responsables de desencadenar los mecanismos de resistencia y tolerancia a las quinolonas. Material y métodos. En el presente trabajo hemos estudiado la implicación de los mecanismos de reparación de DSBs en la sensibilidad a las quinolonas: reanudación de horquillas de replicación paradas dependiente de recombinación (RFR), inducción de la respuesta SOS, reparación por síntesis translesional (TLS) y escisión de nucleótidos (NER). Para ello, en los laboratorios de la Universidad Europea de Madrid, se han analizado las concentraciones mínimas inhibitorias (CMIs) de tres quinolonas diferentes en mutantes procedentes de varias colecciones de cultivos tipo de Escherichia coli. Resultados. Mutantes en recA, recBC, priA y lexA mostraron una disminución significativa de la CMI a todas las quinolonas. No se observaron cambios significativos en estirpes mutantes en los mecanismos de reparación por TLS y NER. Discusión. Estos datos indican que, en presencia de quinolonas, los mecanismos de RFR y la inducción de la respuesta SOS estarían implicados en la aparición de mecanismos de sensibilidad a quinolonas (AU)

Introduction. Quinolones are one of the types of antibiotics with higher resistance rates in the last years. At molecular level, quinolones block type II topoisomerases producing double strand breaks (DSBs). These DSBs could play a double role, as inductors of the quinolone bactericidal effects but also as mediators of the resistance and tolerance mechanisms. Material and methods. In this work we have studied the molecular pathways responsible for DSBs repair in the quinolone susceptibility: the stalled replication fork reversal (recombination-dependent) (RFR), the SOS response induction, the translesional DNA synthesis (TLS) and the nucleotide excision repair mechanisms (NER). For this reason, at the European University in Madrid, we analysed the minimal inhibitory concentration (MIC) to three different quinolones in Escherichia coli mutant strains coming from different type culture collections. Results. recA, recBC, priA and lexA mutants showed a significant reduction on the MIC values for all quinolones tested. No significant changes were observed on mutant strains for TLS and NER. Discussion. These data indicate that in the presence of quinolones, RFR mechanisms and the SOS response could be involved in the quinolone susceptibility (AU)