Banca de QUALIFICAÇÃO: MARIA EDUARDA TENORIO OLIVEIRA

Uma banca de QUALIFICAÇÃO de MESTRADO foi cadastrada pelo programa.
STUDENT : MARIA EDUARDA TENORIO OLIVEIRA
DATE: 28/09/2021
TIME: 14:00
LOCAL: google meet
TITLE:

MULTI-OMIC ANALYSIS OF THE GUT MICROBIOME IN RATS WITH LITHIUM-PILOCARPINE INDUCED TEMPORAL LOBE EPILEPSY

KEY WORDS:

gut-brain-axis, microbiota, metabolome, epilepsy

PAGES: 65
BIG AREA: Ciências Biológicas
AREA: Genética
SUBÁREA: Genética Animal
SUMMARY:

Evidence supports that the gut microbiota and bacteria-dependent metabolites influence the maintenance of epileptic brain activity. However, the alterations in the gut microbiota between epileptic versus healthy individuals are poorly understood. We used a multi-omic approach to evaluate the changes in the composition of gut bacteriome as well in the fecal metabolomic profile in rats before and after being submitted to Status Epilepticus (SE)-induced Temporal Lobe Epilepsy (TLE). The 16S ribosomal RNA (rRNA) sequencing of fecal samples coupled to bioinformatic analysis revealed taxonomic, compositional, and functional shifts in epileptic rats. The species richness (Chao1 index) was significantly lower in the post-TLE group, and the ß-diversity analysis revealed clustering separated from the pre-TLE group. The taxonomic abundance analysis showed a significant increase of Desulfobacterota phylum and a decrease of Patescibacteria. The DESEq2 and LEfSe analysis resulted in 18 genera significantly enriched between pos-TLE and pre-TLE groups at the genus level. We observed that epileptic rats present a peculiar metabolic phenotype, including a lower concentration of D-glucose and L-lactic and a higher concentration of L-glutamic acid and glycine. The microbiota-host metabolic correlation analysis showed that the genera differentially abundant in pos-TLE rats are associated with the altered metabolites, especially the proinflammatory Desulfovibrio and Marvybiatria, which were enriched in epileptic animals and positively correlated with these excitatory neurotransmitters and carbohydrate metabolites. Therefore, our data support the notion that post-SE dysbacteriosis contributes to the development of epilepsy by enhancing chronic inflammation, an excitatory-inhibitory imbalance, and/or a metabolic disturbance.  

BANKING MEMBERS:
Presidente - 2579081 - DANIEL LEITE GOES GITAI
Interno - 1974414 - OLAGIDE WAGNER DE CASTRO
Externa à Instituição - LUCIANA CAMPOS PAULINO - UFABC