Spinal cord injury (SCI) counts about 17,000 new cases each year in the United States. Since axons lose the competence to regenerate in adult mammals, SCI can lead to permanent neurological damages with dramatic personal, social and economic impacts. The long-term deficit of SCI results first from the type of insult and then from the secondary phase that includes many pathophysiological events. Among these, inflammation and epigenetic factors play a crucial role in the recovery of neuron connections. Variations in epigenetic and immune contribution, in turn, depend on age and health status as well as to microbiota profile of individuals at the time of, or consequent to SCI. Indeed, gut microorganisms, highly influence the immune system, but also produce bioactive substances such as folates, butyrate and acetate that participate to the epigenetic processes. Interestingly, variations in the profile of microbiota and bioactive substances have been described in patients with neurologic intestine because of SCI. Recently, different approaches, including stem cell therapy, use of biomaterial and laser therapy, have been proposed for neuronal regeneration after SCI but they are still far from resolutive interventions. As the complexity of pathophysiological processes of the secondary phase can deeply condition the success of regeneration, we provide a landscape of microbiota-epigeneticimmune modulation of neurological recovery predisposition or prevention. We discuss most of data about epigenetics (microRNAs, circulating microRNAs and chromatin remodelling) after SCI in animal models as well as microbiome profile of patients with SCI. We also propose a bioinformatics approach to compare "comics" data (gut microbiome, circulating microRNAs and inflammatory profiles) of patiens with SCI before and after laser therapy to evaluate and improve laser induced neuroregeneration.
BIOINFORMATIC INTEGRATION OF "OMICS" DATA TO EVALUATE AND IMPROVE LASER INDUCED NEUROREGENERATION AFTER SCI: AN OVERVIEW in Abstracts Laser Florence 2017
Mezzelani;Cupaioli F;Sicurello F;Milanesi L
2017
Abstract
Spinal cord injury (SCI) counts about 17,000 new cases each year in the United States. Since axons lose the competence to regenerate in adult mammals, SCI can lead to permanent neurological damages with dramatic personal, social and economic impacts. The long-term deficit of SCI results first from the type of insult and then from the secondary phase that includes many pathophysiological events. Among these, inflammation and epigenetic factors play a crucial role in the recovery of neuron connections. Variations in epigenetic and immune contribution, in turn, depend on age and health status as well as to microbiota profile of individuals at the time of, or consequent to SCI. Indeed, gut microorganisms, highly influence the immune system, but also produce bioactive substances such as folates, butyrate and acetate that participate to the epigenetic processes. Interestingly, variations in the profile of microbiota and bioactive substances have been described in patients with neurologic intestine because of SCI. Recently, different approaches, including stem cell therapy, use of biomaterial and laser therapy, have been proposed for neuronal regeneration after SCI but they are still far from resolutive interventions. As the complexity of pathophysiological processes of the secondary phase can deeply condition the success of regeneration, we provide a landscape of microbiota-epigeneticimmune modulation of neurological recovery predisposition or prevention. We discuss most of data about epigenetics (microRNAs, circulating microRNAs and chromatin remodelling) after SCI in animal models as well as microbiome profile of patients with SCI. We also propose a bioinformatics approach to compare "comics" data (gut microbiome, circulating microRNAs and inflammatory profiles) of patiens with SCI before and after laser therapy to evaluate and improve laser induced neuroregeneration.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.