Jeffrey Gordon

I heard a talk by Dr. Jeffrey Gordon, not Jeff Gordon, for those of you wondering. I was pretty excited about the talk because Dr. Gordon has been putting out some very interesting work concerning the human microbiome and the role of microbial communities in our gut in determining how the host responds to its environmental conditions and diseases.

The talk was very well attended, a testament to the interest in this new field. Dr. Gordon, as seems to be the custom nowadays, introduced the concept that we are more bacterial than eukaryotic, at least by sheer number of cells. I think he mentioned we are 90% microbial and 10% “us” and referred to the collective organism as a supra-organism.

The largest diversity of microorganisms living in our body are located in our gastrointestinal tract. Dr. Gordon alluded to the fact that the modern world with the ability to travel from one place to another, the exposure to many different kinds of foods and the 60 years in which humans have been regularly using antibiotics can really affect the diversity of bacteria in our gut.

2 out of the 100 phyla of bacteria known dominate. These are the firmicutes and the bacteroidetes. There are 8 others in smaller proportion. There is at least one Archaeon. There might be more phages than bacteria in our gut!

Pseudomonas aeruginosa and microbial endocrinology

I recently presented the “Recognition of intestinal epithelial HIF-1a activation by Pseudomonas aeruginosa” by Patel et al. in a journal club discussion.  This group at the University of Chicago led by Eugene Chang and John C. Alverdy try to understand why P. aeruginosa seems to become very active in the intestines after certain surgical procedures. Their previous work described how a laparotomy (opening of the chest cavity) did not induce mortality in mice injected with PA in the cecum, while a partial hepatectomy followed by the injection caused 100% mortality. They reasoned that surgical stress made the bacteria more active (i.e. pathogenic). They focus on a gene that is important for PA’s initial opportunistic adherence called PA-I lectin/adhesin. An interesting paper in Science, which made me look into this group, shows that IFNg, an inflammatory cytokine, can bind to a surface protein of the bacterium and induce changes in transcription. They’ve also published about the effects of dynorphin, an endogeous opioid, on the bacteria’s gene expression.  In this paper, they show that hypoxia, common during surgery, sets off a chain of events that can activate PA.