The HPI Division needs your Science Art: Dr. Borden Lacy inspired a motion to make our corridors more welcome to us and to our visitors! At the beginning of summer labs on the fourth and fifth floor of PMI got together for a cathartic mission that left rooms spotless and spirits high. Now it is time for our WALLS: We would like to ask for each laboratory throughout the division (not just the 4th and 5th floors) to submit a high resolution image (be it microscopy, IMS, crystal structure, FROG, Wasp, you get the gist) so that we can print it in poster format, frame it and use it to decorate the hallways of HPI division labs. This will be a great way to introduce who we are and what we do to visitors, new students and other colleagues from different disciplines. Think about it as a parallel to the "Life Magnified" Exhibit now on display at the IAD International Airport in DC:(http://www.nigms.nih.gov/education/lifemagnified/Pages/default.aspx).
Please submit your images to Helen Chomicki (helen.chomicki@vanderbilt.edu) by November 10, 2014.
HPI Division Meeting: October 28, 2014 at 3pm, MCN A5305. Chalk-Talk, Chris Aiken, Ph.D.
2nd Friday Happy Hour: 10/10/14 at MCN A5305, 4:00pm - Hosted by the Dermody and Rollins-Smith labs.
Featured Publication:
"CD8αα(+) Innate-Type Lymphocytes in the Intestinal Epithelium Mediate Mucosal Immunity."
Van Kaer, L. et al., Immunity 2014; 41(3):451-64
In this report, Van Kaer and colleagues describe an innate lymphoid population closely associated with the intestinal epithelium. These cells, called iCD8α, are TCR-negative lymphoid cells that express the CD8a homodimer.
iCD8a cells exhibit innate functional characteristics such as the capacity to engulf and kill bacteria.
Van Kaer et al., used a murine model to localize these cells and track their lineage, discovering that iCD8a cells depend on IL-2Rγc, IL-15, and H2-T3 for development and maintenance.
The authors then demonstrated that this population of cells is also found in humans and it is significantly depleted in infants with necrotizing colitis, compared to age-matched controls, suggesting a potential role for this cell population in immune responses associated with the intestinal epithelium.
Prior to this study, very little was known about TCR－ lymphoid cells expressing CD8α homodimers.
Have you ever wondered where do those virulence genes come from?
This was the topic of an invigorating seminar given by Dr. Stanley Maloy, the keynote at the Midwest Microbial Pathogenesis Conference, held in Chicago, IL last month. Dr. Maloy’s presentation gave a synopsis of the re-emergence of old infections, as well as the emergence of new “flavors” of pathogens, such as the Shiga-toxin producing E. coli O104:H4. Highlights of his talk included some of his published work with metagenomic studies of the microbiomes from a variety of environments. These studies have shown that many of the exotoxin genes carried by bacterial pathogens are phage-encoded, thus, when phage that carry these genes infect an appropriate bacterial host, the bacterium undergoes lysogenic conversion, converting the bacterium from an avirulent strain to a pathogen that can cause human disease. This was confirmation of “old news”. What is striking from these studies, which were primarily carried out by environmental biologists, is the fact that exotoxin-encoding phage are commonly found in environments that lack the cognate bacteria commonly associated with the specific toxin-mediated disease and have been found to be associated with alternative environmental bacterial hosts! Which leads to the hypothesis that these “virulence” genes serve a beneficial role in the ecology of these environmental bacteria. Transfer of the exotoxin genes between bacteria has been shown to occur in marine environments, animal and human intestines and sewage treatment plants. Dr. Maloy then went on to remind the audience about the increasing (and inevitable) interference with natural habitats, the ongoing climate changes and how these events are shaping the ecology of microbes and the transfer of genetic material to bacteria that interact (parasitically or mutualistically) with humans.
Other MMPC highlights included:
An oral presentation by our very own Michelle LaFrance from the Lacy lab, who was selected from the abstracts to present her work to identify the epithelial cell receptor responsible for C. difficile TcdB-mediated necrosis. Congratulations Michelle!
A significant number of HPI researchers and trainees presenting their work during the poster sessions: Erin Breland (Hadjifrangiskou); Ramya Chandrasekaran (Lacy); Kathryn Haly (Gaddy); Neal Hammer (Skaar); Lillian Johnson (Skaar); Heather Kroh (Lacy); Brittany Mortensen (Skaar).
What are your thoughts? Feel free to muse by sending us an email (maria.hadjifrangiskou@vanderbilt.edu, helen.chomicki@vanderbilt.edu)
