Guest guest Posted June 23, 2007 Report Share Posted June 23, 2007 God, I hope people pay attention to this study. Thanks, Roy. penny royx31 <roysno@...> wrote: http://tinyurl.com/3c9c8uRoy Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 23, 2007 Report Share Posted June 23, 2007 Penny, You're welcome.I'm not sure if that URL will remain active, so I'll just post the article: Reported June 18, 2007 Bacteria Sneaks and Hides in Cells (Ivanhoe Newswire) -- Researchers have found Staphylococcus aureus bacteria may elude the immune system by sneaking into cells and hiding out to avoid detection. Researchers from University Hospital of Geneva in Switzerland and the Institute of Food Research in Norwich, UK, embarked on a study to find out just what S. aureus does in human lung epithelial cells. S. aureus is a major cause of human and animal infections. Just like a villainous shape-shifter, shortly after S. aureus entered the lung cells, researchers found the bacteria's gene expression profile changed dramatically. They found the gene expression for bacterial metabolic functions and transport actually shut down, leaving the infectious bug in a dormant state. At the same time, researchers discovered the production of toxins that can kill epithelial cells became strictly controlled to limit cell damage. Then, the mechanisms that help the bacteria survive resumed. Results of the study could pave the way to a better understanding of these types of infections as well as help researchers come up with better antibacterial drugs to fight them. It could also help them better understand what goes on at the molecular level that makes S. aureus so persistent. Researchers say the bacteria can re-surface and cause another infection years after the initial episode was " cured. " Patrice Francois, from University Hospital in Geneva, was quoted as saying, " S. aureus intracellular survival appears related to its capability to adopt a discrete behavior instead of actively duplicating. S. aureus then benefits from natural or programmed cell death to re-emerge and trigger another episode of infection, leading to chronicity. " This article was reported by Ivanhoe.com, which offers Medical Alerts by e-mail every day of the week. To subscribe, click on: http://www.ivanhoe.com/newsalert/. SOURCE: BMC Genomics, June 14, 2007 > http://tinyurl.com/3c9c8u > > Roy > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 24, 2007 Report Share Posted June 24, 2007 Thank you! I use to have this " ivanhoe " web site years and years ago, but after enough comp crashes, it got lost, for good. Thank you so much for giving it back. Its a really great site. And yes, I hope everyone takes that study seriously. ~ Priitaa Hypothyroid Vegetarians: HypothyroidVegetarians > http://tinyurl.com/3c9c8u > > Roy > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 24, 2007 Report Share Posted June 24, 2007 The corresponding paper is free and the preprint PDF is at: http://www.biomedcentral.com/content/pdf/1471-2164-8-171.pdf Penny and Tony, you might be interested as they mention something about staph and refractory chronic rhinosinusitis. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 24, 2007 Report Share Posted June 24, 2007 Weird thing about this paper is that they mention in the intro how staph can either escape from the endosome of a non-pro-phagocytic cell, or remain inside it, or escape after a delay. But I don't see any methods used here (ie, electron microscopy) to find out which one(s) of those possibilities were occuring in their system - although the transcriptome does " look " distinctly more like most of the varmints are endosomal, considering the extreme upregulation of transporters. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 25, 2007 Report Share Posted June 25, 2007 Yeah, that's what I was thinking...;-) penny <usenethod@...> wrote: Weird thing about this paper is that they mention in the intro how staph can either escape from the endosome of a non-pro-phagocytic cell, or remain inside it, or escape after a delay. But I don't see any methods used here (ie, electron microscopy) to find out which one(s) of those possibilities were occuring in their system - although the transcriptome does "look" distinctly more like most of the varmints are endosomal, considering the extreme upregulation of transporters. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 25, 2007 Report Share Posted June 25, 2007 Yeah, the nutritional status of bacteria inside cells is kind of a tough thing to study. There's a lot that isn't known and a lot of details to cover. But generally speaking the endosome/phagosome is nutrient-poor, and the cytosol nutrient-rich. When the bacterium starts sythesizing tons of transporters, it looks like it is having a hard time getting itself fed. Most bacterial transporters are for uptake of nutrients, though a few may be for excretion of wastes, etc. > Yeah, that's what I was thinking...;-) > Weird thing about this paper is that they mention in the intro how > staph can either escape from the endosome of a non-pro-phagocytic cell, > or remain inside it, or escape after a delay. But I don't see any > methods used here (ie, electron microscopy) to find out which one(s) of > those possibilities were occuring in their system - although the > transcriptome does " look " distinctly more like most of the varmints are > endosomal, considering the extreme upregulation of transporters. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 25, 2007 Report Share Posted June 25, 2007 this isn't only for me and penny, everyone on this forum has staphs, and they also have some form of inflammation regardless of the term used, rhinosinusitis, or whatever. Also if you did more than a few swabs you'd definately have a pseudomonal component to boot.So anything describing why we can benefit from antimicrobials, yet have an infection persist, is important to us all. I tend to feel that if we can buy powdered forms of bacteria, just add water and gain five billion organisms. we should accept that we can have infections that persist.. tony > > > The corresponding paper is free and the preprint PDF is at: > > http://www.biomedcentral.com/content/pdf/1471-2164-8-171.pdf > > Penny and Tony, you might be interested as they mention something about > staph and refractory chronic rhinosinusitis. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 25, 2007 Report Share Posted June 25, 2007 something else for you to ponder.If people with strep throat (a nasty bacterium -streptococcus pyogenes) don't normally have a problem day to day until an inflammation cycle starts.What's going on in these cases? tony > > > The corresponding paper is free and the preprint PDF is at: > > http://www.biomedcentral.com/content/pdf/1471-2164-8-171.pdf > > Penny and Tony, you might be interested as they mention something about > staph and refractory chronic rhinosinusitis. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 28, 2007 Report Share Posted June 28, 2007 I'm not sure exactly what you mean? What's an inflammation cycle? I don't know much about S py or strep throat, but I was told in my Intro Micro lecture (lo these many years ago) that S py can be isolated from the throats of ~10% of normal people walking around, at any given time. Why they don't always behave virulently, I don't know. Whether anyone is permanently colonized, I also don't know. With Staph aureus, some asymptomatic people are colonized permanently and some transiently. > something else for you to ponder.If people with strep throat (a > nasty bacterium -streptococcus pyogenes) don't normally have a > problem day to day until an inflammation cycle starts.What's going on > in these cases? > tony Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 29, 2007 Report Share Posted June 29, 2007 What I'm noticing is that bad bacteria are calm until a set of circumstances arises to bring out the worst in them.People with bad strep bacteria do fine until something throws the switch in the bacteria to make it angry.It's this switchability that's possably more a problem and by adding more resistant genes to a bacterium your increasiing it's ability to be switched. Another way of looking at this is that some bacteria are only found on there own, possably due to being able to switch on and take out a competitor. A healthy person wityh no sinus inflammation can have a harmony of bacteria and fungus's and the cfs people have pseudonomas , staph areus and staph epi.. Yet another way of looking at this switching is steven johnson syndrome. Something will annoy the bacterium and they'll throw out a shit load of toxins that will exfoliate you like a third degree burns patient. > > > I'm not sure exactly what you mean? What's an inflammation cycle? > > I don't know much about S py or strep throat, but I was told in my > Intro Micro lecture (lo these many years ago) that S py can be > isolated from the throats of ~10% of normal people walking around, at > any given time. Why they don't always behave virulently, I don't know. > Whether anyone is permanently colonized, I also don't know. With Staph > aureus, some asymptomatic people are colonized permanently and some > transiently. > > > > something else for you to ponder.If people with strep throat (a > > nasty bacterium -streptococcus pyogenes) don't normally have a > > problem day to day until an inflammation cycle starts.What's going on > > in these cases? > > tony > Quote Link to comment Share on other sites More sharing options...
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