Unfortunately, I will not be able to attend to AHS this year, due to some unexpected financial and academic (damn single molecules!) problems. I was looking forward to meet most of the “paleosphere” and discuss about science with very bright people. I hope I can make it in 2013.
I have been very busy working on the lab, teaching biochemistry and cell biology in Med School and doing a post-graduate diploma in basic and clinical immunology. Because of this, I have had little time for reading carefully studies which are not related to my thesis, and in my short spare time I wanted to let my brain “rest” a little bit, although I have read some (but not as much as I would like to). Accordingly, I haven’t had any time to update the blog. Nonetheless, I have an almost finished post on dietary fats and immune function, which may raise some controversy in the “low carb” community. I want to finish and publish this post once for all (it has been almost finished for almost one month now). I might add some information that I was keeping for my AHS talk (see bottom of the post).
In the meantime, and to make something productive out of this post, here are some studies I have found interesting lately (not all related to the topic of my blog, by the way).
Inducing myocardial infarction (MI) in NOD mice (non-obese diabetic mice) triggers the development of severe post-infarction autoimmune syndrome characterized by lymphocyte infiltration to the myocardium, infarct expansion, and autoantibody and Th1 type response to cardiac alpha-myosin. 83% of a sample of post-myocardial infarction T1D patients showed positive tests for autoantibody against cardiac proteins.
|Post-infarcted myocardium from NOD mice showed extensive lymphocytic infiltrates resembling those from pancreas islets, and extended into the non-infarcted myocardium (left image). Normal mice (B6) showed no infiltration nor expansion, but normal infarct healing and scar formation (right image). © 2012 American Association for the Advancement of Science. All Rights Reserved.|
|WD-milk promotes alopecia. Copyright © 2012 by Cold Spring Harbor Laboratory Press|
|Fasting improves metabolic alterations induced by high-fat diets in mice. Copyright © 2012 Elsevier Inc. All rights reserved.|
Iliev, et al. show that although bacteria are a very important (and the major component) for the gut microbiota, there are also other organisms which play an essential role in the host's health. This is the case for some fungi, which interact with the host through dectin-1 receptors, inducing a Th17-type immune response. Mice lacking dectin-1 are susceptible to DSS-induced colitis, and show an abnormal inflammatory response. Inducing colitis altered the mycobiome, and treatment with fluconazole (antifungal) ameliorated inflammation. Analysis of the mouse fungal microbiome revealed that 65.2% of the sequences identified corresponded to Candida tropicalis, an opportunistic pathogen. Their results showed that dectin-1 restricts its body localization to the intestinal lumen (so there is no invasion of inflamed tissues). Colitis also increased the proportion of Candida and Trichosporon (opportunistic pathogens) and reduced the levels of Saccharomyces (non-pathogenic). Supporting their hypothesis, they found an haplotype in the CLEC7A gene (human dectin-1 gene) which was correlated with severe forms of ulcerative colitis, but not with non-severe manifestations.
|Fungi levels are an important part of the murine gut microbiota. This probably occurs also in humans. © 2012 American Association for the Advancement of Science. All Rights Reserved.|
The mechanism by which phages transfer their DNA to bacteria has been a key question for decades. Using a single-molecule system with two different strains of lambda phage (differing in genome length), Van Valen, et al. found that the time it takes for lambda phage to transfer its DNA to a single E.coli cell takes 5 minutes (with high cell-to-cell variability and sometimes showing long pauses), compared to what it is seen in vitro, where the process takes roughly 10 seconds. The in vivo velocity of DNA ejection seemed to be determined by the amount of DNA ejected, not by the amount of DNA left in the viral capsid (which is what has been seen in vitro). The method utilized by the authors is theoretically simple (see figure). They stained viral DNA while still in the capsid with a cyanide dye (SYTOX orange), after which excessive dye is washed out. The stained phages are then briefly bound to bacterial cells, which are pipetted into a flow chamber. After washing again with buffer, the sample is imaged with time-lapse bright-field and fluorescence microscopy. The ejection of DNA is measured by comparing the fluorescence intensity inside the phage capsid to that of the bacterial cell: a loss of fluorescence inside the capsid with a concomitant increase in the cell represents DNA translocation.
|Copyright © 2012 Elsevier Inc. All rights reserved.|
|Fluorescence imaging of the process of DNA ejection to a single E.coli cell. Copyright © 2012 Elsevier Inc. All rights reserved.|
** It was also lower in PUFA (12.2% in WD vs. 61.8% in chow), but much higher in sucrose (152.8g/kg in WD vs. 0g/kg in chow).
*** Nevertheless, some inflammatory cytokines were still increased compared to control.
PD. I wanted to make public my thanks to the AHS organizers for their help with paper work and answering any question I had immediately. I feel very bad for cancelling my talk, specially after their help. Also, I want to thank to everyone who supported my talk me via donations. Please, if anyone who donated wants a refund, send me an email. For anyone who was expecting my talk, I will compensate it with more information on my blog. First, I will finish and post my second post on my nutrition immunotherapy protocol, and second, I will add a new page to the blog with schematic and didactic diagrams made for my presentation. They will be available for free to everyone.
Iliev ID, Funari VA, Taylor KD, Nguyen Q, Reyes CN, Strom SP, Brown J, Becker CA, Fleshner PR, Dubinsky M, Rotter JI, Wang HL, McGovern DP, Brown GD, & Underhill DM (2012). Interactions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis. Science (New York, N.Y.), 336 (6086), 1314-7 PMID: 22674328