Webinar: MyD88 signaling in intestinal epithelial cells shapes the composition of the gut microbiota
Attend a 30 minute webinar with Dr. Charlotte Kaetzel from the University of Kentucky School of Medicine on "MyD88 signaling in intestinal epithelial cells shapes the composition of the gut microbiota." Dr. Kaetzel and colleagues have identified major microbiome composition changes in the intestine of mice with a deletion in the critical signaling molecule involved in maintaining the intestinal epithelial barrier, MyD88. Their work was published in the journal Mucosal Immunology.
When: May 23, 2012, 9:00am PT/12:00pm ET
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The Microbiome: Keystone Symposia Quick Recap
This spring, the Keystone Symposia meeting on The Microbiome at the Keystone Resort in Colorado was host to a fantastic collection of speakers and posters focused on understanding the mechanisms underpinning the host-microbiota relationship and how they impact health and disease.
There were several key themes that sparked our interest here at Second Genome. Significant effort is being placed on understanding how the microbiota modulates the inflammatory process and the implications for chronic inflammatory diseases. The intestinal immune system has many interdependent players; research presented at the meeting highlighted the role of Toll-like and Nod receptors in innate immunity with relevancy for novel treatments for inflammatory bowel disorders and metabolic disease. The role of the innate immune system in modulating the adaptive response to intestinal bacteria was explored in relation to maintaining gut homeostasis. Research demonstrating how commensal bacteria exploit signaling receptors of the innate immune system to promote colonization was also presented. Several speakers highlighted the importance of the intestinal epithelial barrier and associated mucus layers in protecting the intestine from infiltration of bacteria that often results in inflammation.
Several talks highlighted the importance of "keystone" microbial species. These low abundance species have disproportional effects on the microbiota community through mechanisms that may include production of metabolites used by other bacteria to survive. Interesting work on certain probiotic strains found that, counterintuitively, whole bacteria caused an increase in inflammation whereas supernatants from these bacteria had beneficial effects. This type of work sets up an important avenue for exploration into "post-biotics" where microbial products such as metabolites or enzymes are explored as novel drug candidates. As with many of the recent leaps in genomics, many expressed the challenges associated with integrating information from microbial profiling and functional studies, but the field is clearly focused on developing a holistic view of these complex microbial systems.
New Publication on Signature of Intestinal Barrier Loss
Second Genome's Microbiome Signature Discovery services have been cited in a new publication in the prestigious journal Mucosal Immunology. The Kaetzel laboratory at the University of Kentucky College of Medicine found that major microbiome composition changes occurred in the intestine of mice with a deletion of a critical signaling molecule involved in maintaining the intestinal epithelial barrier, MyD88.
Using Second Genome's PhyloChip assay, the team found that MyD88 deficient mice have increased levels of bacteria from the Proteobacteria phylum and decreased levels of of bacteria from the Bacteroidetes phylum. They highlight that IBD patients have similar gut microbiota composition changes and attribute these alterations to increased intestinal permeability, decreased production of antimicrobial peptides, and aberrant SIgA responses. Analysis of their samples identified four signature bacterial OTUs in the candidate division TM7, whose increased abundance was characteristic of the altered microbiota of MyD88 deficient mice. They make the important connection that increased abundance of TM7 bacteria have been reported in humans with oral inflammation, IBD and mice deficient in the NLRP6 inflammasome, accompanied by the development of spontaneous intestinal inflammation and increased susceptibility to DSS-induced colitis. Their work suggests that epithelial MyD88 signaling is required to protect against abnormal expansion of specific members of the gut microbial community.
Read the publication here.
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