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Hello TWiMsters! I recently discovered the trifecta that is the TWi series, and now I can’t get enough of your discussions of all things micro. For graduate students like myself, keeping up with the scientific literature can all too easily become just a means for cramming information into our brains that we feel we “should” know. Not only do your shows keep my mind stimulated and expose me to scientific papers that I might not otherwise read, but the informal and enthusiastic nature of the programs are just the slap in the face I need to crawl out from under the stack of papers, and remind me that I actually love to learn about science and to think about the various implications that a particular finding or result might have. After listening to your conversational discussion format and your fantastic insights that tie together the biology of the organism (or virus – are viruses organisms?) with the environment, host, experimental techniques etc., I am finding new clarity in the way that I think about scientific problems and evaluate scientific papers. I can’t commend you enough for what you do. Formal presentations of scientific findings are a dime a dozen - listening to world-class scientists “chat” amongst themselves about current topics in microbiology is an invaluable resource that few people really ever get a chance to do, until now. THANK YOU!
On a scientific note, I was recently listening to TWIM #43 and your discussion on the stable formation of caveolae in in E. coli. It was mentioned that it had previously been thought that stable caveolae formation in eukaryotic cells requires cholesterol, to which Michael replied that “there is [no cholesterol] in our friends the bacteria”. Although this was and is true in the context of E. coli and the paper’s findings, I think it is worth pointing out that there are several described examples of free cholesterol and cholesterol-containing glycolipids in bacterial outer membranes – namely in Helicobacter, Mycoplasma, Ehrlichia, Anaplasma, Brachyspira, and Borrelia species. In Borrelia burgdorferi, cholesterol containing compounds have been shown to form organized lipid rafts both in culture and in animal-derived organisms, with physical properties similar to that in eukaryotic membranes. A recent paper published in PLOS Pathogens in January of 2013 utilized fluorescent and radiolabeled cholesterol to demonstrate that B. burgdorferi extracts cholesterol from the plasma membrane of eukaryotic cells, and that prokaryotic cholesterol-glycolipids can be transferred to epithelial cell membranes through both a contact dependent mechanism (using direct attachment) and a contact independent method (through released outer membrane vesicles). I highly recommend looking in to this story (maybe as a TWIM topic?), as it provides a shift in the thinking about lipid rafts, expanding their biological relevance to prokaryotes, and could have implications for the evolution of the eukaryotic cell membrane structure. Additionally, transfer of antigenic lipids from bacteria to host cells could play a role in pathogenesis - having multiple consequences for the host immune response and potentially contributing to heightened inflammation, and perhaps even direct targeting of the cells themselves by immune effectors. I’ve provided the citations and Pubmed links to a few papers on the B. burgdorferi story below, but also recommend digging into the story for H. pylori.
I’ve rambled enough for now, I should run – I’ve got to get to iTunes to write a good review or two…
LaRocca TJ, Crowley JT, Cusack BJ, Pathak P, Benach J, et al. (2010) Cholesterol lipids of Borrelia burgdorferi form lipid rafts and are required for the bactericidal activity of a complement-independent antibody. Cell Host Microbe 8: 331–342.http://www.ncbi.nlm.nih.gov/pubmed/20951967/
Crowley JT, Toledo AM, LaRocca TJ, Coleman JL, London E, et al. (2013) Lipid Exchange between Borrelia burgdorferi and Host Cells. PLoS Pathog 9(1): e1003109. http://www.ncbi.nlm.nih.gov/pubmed/23326230
Department of Veterinary Microbiology and Pathology
Washington State University
“The truth is incontrovertible. Malice may attack it, ignorance may deride it, but in the end, there it is.”
- Winston Churchill
During TWiM#46 it was discussed that spores are able to sense peptidoglycan that has been shed by other bacteria. I would like to know, are the spores able to differentiate between the peptidoglycan that is shed by growing bacterial neighbours and the peptidoglycan lost during lysis.
University of Victoria, BC, Canada
Jon Dworkin answers:
Excellent question! If this any indication, your listeners are really paying attention!
Spores are able to differentiate between peptidoglycan fragments generated from growth and those generated by lysis since these processes in fact produce different PG fragments. Those resulting from lysis are thought to be produced largely by lytic transglycosylases which generate PG fragments containing an anhydro (non-reducing) end, whereas fragments produced in growth do not contain this group. In collaboration with Shariar Mobashey, an excellent PG chemist at Notre Dame, we demonstrated that synthetic muropeptides containing an anhydro group do not stimulate growth but synthetic muropeptides that lack this group are able to stimulate spore germination. Thus, spores can differentiate between cells in the milieu that are lysing versus those that are growing.
Finally, I can send an intelligent comment (re: TWiM #51) ...
Dear esteemed doctors,
I am sincere in this appellation as one of your many listeners who depend upon your unbiased fact finding and enlightening delivery to both educate and debunk with the latest information.
You have often remarked on the contradiction of the numerous pathogenic bacteria in common public areas while you as individuals do not feel endangered. In commenting on a letter read on TWIM 72 you mentioned the "cloud" of toilet-originating microbes created with every flush, yet a lack of evidence of resulting disease. It comes up also in regular mentions of door knobs, railings, phones and other public conveniences. Often this is attributed to the protection provided by a healthy immune system.
My question is whether the mechanism of microbial balance achieved in the human microbiome should be applied to understanding the forces at work in these external environments. Might our Linus-like microbial cloud function like the often mischaracterized schmutzdecke which purifies much of our drinking water?
Analyzing the potential health affects of environmental microbes apart from the greater human and environmental microbiomes seems a bit like analyzing the path of stars orbiting the earth. Am I wrong to assume that the microbial community of the toilet, room air, hands, nose and mouth have a significant impact on the danger from most of the individual microbes within those communities?
It's 252 degrees absolute, (or minus cold aught six on the Retrograde scale) this morning in sunny Connecticut.
A sincere thanks to you all for your dedication to TWIX. The world is listening to you more intently every day, and better for it.