Targeting Microbiota 2020 will be a Virtual and In-Person Congress

We have been closely following updates and evolving guidance from local, national and global agencies for COVID-19. There is still much uncertainty around the coronavirus, and how long our communities may be impacted by the pandemic, but it seems certain that decisions about how we work, travel and gather together will continue to be influenced for weeks and months still to come. Today, we have made the decision to combine In-Person and Virtual conference.

 

If you cannot attend in-person or virtual due to the restriction and time zone difference, you can access on-demand videos to this entire event, including synced audio/video and slides.

All posters will be in PDF format. You can visit them, upload and interact directly with the poster presenter. You can also exchange with speakers via direct or private exchange during the conference.

We will keep you informed of any new decision.

Using a mouse model of necrotizing enterocolitis (NEC) -- a potentially fatal condition that causes a premature infant's gut to suddenly die

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Researchers at Johns Hopkins say they have uncovered the molecular causes of the condition and its associated brain injury.

Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease of the premature infant. One of the most important long-term complications observed in children who survive NEC early in life is the development of profound neurological impairments. However, the pathways leading to NEC-associated neurological impairments remain unknown, thus limiting the development of prevention strategies. We have recently shown that NEC development is dependent on the expression of the lipopolysaccharide receptor Toll-like receptor 4 (TLR4) on the intestinal epithelium, whose activation by bacteria in the newborn gut leads to mucosal inflammation. Here, we hypothesized that damage-induced production of TLR4 endogenous ligands in the intestine might lead to the activation of microglial cells in the brain and promote cognitive impairments. We identified a gut-brain signaling axis in an NEC mouse model in which activation of intestinal TLR4 signaling led to release of high-mobility group box 1 in the intestine that, in turn, promoted microglial activation in the brain and neurological dysfunction. We further demonstrated that an orally administered dendrimer-based nanotherapeutic approach to targeting activated microglia could prevent NEC-associated neurological dysfunction in neonatal mice. These findings shed light on the molecular pathways leading to the development of NEC-associated brain injury, provide a rationale for early removal of diseased intestine in NEC, and indicate the potential of targeted therapies that protect the developing brain in the treatment of NEC in early childhood.

 

News source: www.ncbi.nlm.nih.gov

Microbiota in the Press & Media

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