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Zonulin,leaky gut and blood brain barrier articles

Discussion in 'Adrenal Rx and Leaky Gut Rx' started by chocolate, Apr 9, 2012.

  1. chocolate

    chocolate Silver

    [h=1]Metal Chelation and Inhibition of Bacterial Growth in Tissue Abscesses[/h]http://www.sciencemag.org/content/319/5865/962.abstract





    Bacterial infection often results in the formation of tissue abscesses, which represent the primary site of interaction between invading bacteria and the innate immune system. We identify the host protein calprotectin as a neutrophil-dependent factor expressed inside Staphylococcus aureus abscesses. Neutrophil-derived calprotectin inhibited S. aureus growth through chelation of nutrient Mn2+ and Zn2+: an activity that results in reprogramming of the bacterial transcriptome. The abscesses of mice lacking calprotectin were enriched in metal, and staphylococcal proliferation was enhanced in these metal-rich abscesses. These results demonstrate that calprotectin is a critical factor in the innate immune response to infection and define metal chelation as a strategy for inhibiting microbial growth inside abscessed tissue.
     
  2. KiwiLauren

    KiwiLauren Gold


    OK, this makes good sense (and yes, you are super smart, evidenced by your super smart guesses!). This is only tangentially related, but I think supports your theory... today a friend and I were talking about changes we've experienced since going paleo (she only does the diet and circadian stuff, not CT yet) and one of them was that neither of us stink/need deodorant any more. She said she only realised that this happen AFTER she stopped eating all fruits/sugars. I think this 'imposter' syndrome does raise toxicity and potentially act as a virus, opening the emergency exit you suggest. Hence the smell.
     
  3. chocolate

    chocolate Silver

    Gut Microbiota Transplantation May Prevent Development of Diabetes and Fatty Liver Disease

    http://www.sciencedaily.com/releases/2012/04/120419091026.htm





    ScienceDaily (Apr. 19, 2012) — Exciting new data presented April 18 at the International Liver CongressTM 2012 shows the gut microbiota's causal role in the development of diabetes and non-alcoholic fatty liver disease (NAFLD), independent of obesity1. Though an early stage animal model, the French study highlights the possibility of preventing diabetes and NAFLD with gut microbiota transplantation -- the engrafting of new microbiota, usually through administering fecal material from a healthy donor into the colon of a diseased recipient.2

    In the 16 week study, two groups of germ free mice received gut microbiota transplants; one set from donor mice displaying symptoms of insulin resistance and liver steatosis (responders), the other from normal mice (non responders). The donor mice were selected due to their response to being fed a high fat diet.



    The germ free group that received microbiota from symptomatic mice (responder receivers -- RR) showed higher levels of fat concentration in the liver as well as being insulin resistant. The germ free group that received microbiota from healthy mice (non-responder-receivers -- NRR) maintained normal glucose levels and sensitivity to insulin.



    EASL Scientific Committee Member Dr Frank Lammert said: "The factors leading to Non-Alcoholic Fatty Liver Disease (NAFLD) are poorly understood, but it is known that NAFLD and Type 2 diabetes are characterized, respectively, by liver inflammation and metabolic disorders like insulin resistance."



    "This study shows that different microbiota cause different metabolic responses in animals. By implanting microbiota from healthy mice, the study authors prevented the development of liver inflammation and insulin resistance, both indications of liver disease and diabetes. Thus, gut microbiota transplants could have a therapeutic role in the development of these diseases."



    The RR mice also showed lower levels of microorganisms than usually found in the healthy gut. Lachnospiraceae was identified as the species most important in developing fatty liver and insulin resistance.
     
  4. chocolate

    chocolate Silver

    http://www.ncbi.nlm.nih.gov/pubmed/22228654

    Lachnoanaerobaculum a new genus in Lachnospiraceae; characterization of Lachnoanaerobaculum umeaense gen. nov., sp. nov., isolated from human small intestine, Lachnoanaerobaculum orale gen. nov., sp. nov., isolated from saliva and reclassification of Eubacterium saburreum (Prevot) Holdeman and Moore 1970 as Lachnoanaerobaculum saburreum comb. nov.





    Abstract



    Two new obligately anaerobic Gram-positive, saccharolytic and non-proteolytic spore-forming bacilli (strain CD3:22 and N1) are described. Strain CD3:22 was isolated from a biopsy of the small intestine of a child with celiac disease and strain N1 from the saliva of a healthy young man. The cells of both strains were observed to be filamentous with lengths of approximately 5 to >20 µm, some of them curving and with swellings. The novel organisms produced H2S, NH3, butyric acid and acetic acid as major metabolic end products. Phylogenetic analyses, based on comparative 16S rRNA gene sequencing, revealed close relationships (98 % sequence similarity) between the two isolates, as well as the type strain of Eubacterium saburreum CCUG 28089T and four other Lachnospiraceae bacterium/E. saburreum-like organisms. This group of bacteria were clearly different from any of the 19 known genera in the family Lachnospiraceae. While Eubacterium spp. are reported to be non-spore-forming, reanalysis of E. saburreum CCUG 28089T confirmed that the bacterium, indeed, is able to form spores. Based on 16S rRNA gene sequencing, phenotypic and biochemical properties, CD3:22 (CCUG 58757T) and N1 (CCUG 60305T) represent new species of a new and distinct genus, named Lachnoanaerobaculum, in the family Lachnospiraceae [within the order Clostridiales, class Clostridia, phylum Firmicutes]. Strain CD3:22 is the type strain of the type species, Lachnoanaerobaculum umeaense gen. nov., sp. nov., of the proposed new genus. Strain N1 is the type strain of the species, Lachnoanaerobaculum orale gen. nov., sp. nov. Moreover, E. saburreum CCUG 28089T is reclassified as Lachnoanaerobaculum saburreum comb. nov.
     
  5. chocolate

    chocolate Silver

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134041/

    Probiotics in periodontal health and disease



    Received June 12, 2009; Accepted August 23, 2010.



    Apoptosis is yet another proposed mechanism. Probiotics stimulate apoptosis of tumor cells through end product formation.[5] It has also reported to inhibit apoptosis of mucosal cells.[6]

    Probiotic mixture has also been reported to protect epithelium barrier by maintaining tight junction protein expression and prevent apoptosis of mucous membrane.[7
     
  6. chocolate

    chocolate Silver

  7. Trying to follow you chocolate. Great stuff. I'm tyoe A blood and i believe that blood type diet recommends type a be vegetarians. Sounds like a bad call Now where us the zonulin for dummies?
     
  8. chocolate

    chocolate Silver

    http://www.ncbi.nlm.nih.gov/pubmed/22260250



    Ammonia increases paracellular permeability of rat brain endothelial cells by a mechanism encompassing oxidative/nitrosative stress and activation of matrix metalloproteinases.

     
  9. chocolate

    chocolate Silver

    http://www.ncbi.nlm.nih.gov/pubmed/17250680

    Oxidative stress activates protein tyrosine kinase and matrix metalloproteinases leading to blood-brain barrier dysfunction.

    Haorah J, Ramirez SH, Schall K, Smith D, Pandya R, Persidsky Y.

    Source



    Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198-5215, USA. Jhaorah@unmc.edu

    Abstract



    The blood-brain barrier (BBB) formed by brain microvascular endothelial cells (BMVEC) regulates the passage of molecules and leukocytes in and out of the brain. Oxidative stress is a major underlying cause of neurodegenerative and neuroinflammatory disorders and BBB injury associated with them. Using human BMVEC grown on porous membranes covered with basement membrane (BM) matrix (BBB models), we demonstrated that reactive oxygen species (ROS) augmented permeability and monocyte migration across BBB. ROS activated matrix metalloproteinases (MMP-1, -2, and -9) and decreased tissue inhibitors of MMPs (TIMP-1 and -2) in a protein tyrosine kinase (PTK)-dependent manner. Increase in MMPs and PTK activities paralleled degradation of BM protein and enhanced tyrosine phosphorylation of tight junction (TJ) protein. These effects and enhanced permeability/monocyte migration were prevented by inhibitors of MMPs, PTKs, or antioxidant suggesting that oxidative stress caused BBB injury via degradation of BM protein by activated MMPs and by PTK-mediated TJ protein phosphorylation. These findings point to new therapeutic interventions ameliorating BBB dysfunction in neurological disorders such as stroke or neuroinflammation.
     
  10. chocolate

    chocolate Silver

    http://www.ncbi.nlm.nih.gov/pubmed/19241241



     
  11. chocolate

    chocolate Silver

    http://www.ncbi.nlm.nih.gov/pubmed/10901420



    Dietary cod liver oil decreases arachidonic acid in rat gastric mucosa and increases stress-induced gastric erosions.



     
  12. Michael

    Michael Super Moderator


    Dr. Natasha Campbell-McBride, the doctor who specializes in gut health and its relation to psychological problems - see her book on the GAPS diet - believes from her clinical experience that a gut microbiome can get worse over generations. So the grandmother eats a little worse than her ancestors; she passes the microbes on to her daughter (as described above); the daughter maybe eats a bit worse, or is bottle-fed (which also affects the flora), or has a few antibiotic courses - or all three - so the already-damaged flora she initially inherited from her mother gets damaged further. This twice-generationally-damaged flora is what the baby starts with - remember, through swallowing during birth. This, says, Dr. McBride could explain the increase in conditions such as autism, since there is a strong connection between gut-health and how the brain functions.
     
  13. chocolate

    chocolate Silver

    I don't know about any of it any more... the meconimum is in utero and not sterile. The appendix is the safe house.

    I know the fat acts likes its own separate organ and throws signals to the gut flora so your head isn't thinking, it's your fat. Fat, apparently, has lots of feelings. I also know that lots of fat is viral. That's why I like ct. I had a 5lb ab blob that wouldn't go away without cold water. Everything else would.
     
  14. Michael

    Michael Super Moderator

    Well, whatever your fat's done and however "safe" your appendix is, Chris Masterjohn did not say, "genetics determine intestinal flora". That was nowhere in the link you gave.
     
  15. chocolate

    chocolate Silver

    I'm glad someone was paying attention. My apologies for the harm caused.
     

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