Wednesday, August 3, 2011

17 Abstract: Invasion of eukaryotic cells by Borrelia burgdorferi requires β(1) integrins and Src kinase activity

Due to ASM's copyright terms on this journal, it's my understanding that I can't post the entire abstract for this publication here - even though abstracts are pretty much something I have long considered open source and commonly shared. Most scientists do - so to find out that some publishing companies and journals don't even want people to repost abstracts seems... well... strange to me.

How else does one promote their work to other people? I'd consider it free promotion for the full publication!

However, I wanted to share it with you however I could, because I think it's of value:

Invasion of eukaryotic cells by Borrelia burgdorferi requires β(1) integrins and Src kinase activity. Wu J, Weening EH, Faske JB, Höök M, Skare JT. Infect Immun. 2011 Mar;79(3):1338-48. Epub 2010 Dec 20.

Read The Abstract Here:

This abstract relates directly to this post I made recently:

It's about how Lyme disease spirochetes may be able to hide from the immune system inside other cells, especially fibroblasts. The above study is more research related to this topic, so I recommend reading my recent post for background then looking at the above abstract on PubMed.


  1. Reading abstracts like this one gives me a headache after a while.

    To sweeten the pot, let's add this one while we're at it:

    Invasion of human neuronal and glial cells by an infectious strain of Borrelia burgdorferi. Livengood JA, Gilmore RD Jr.
    Centers for Disease Control and Prevention, Division of Vector-borne Infectious Diseases, 3150 Rampart Road, CSU Foothills Campus, Fort Collins, CO 80522, USA.

    Quotes from the above:

    "Further analysis by differential immunofluorescent staining of external and internal organisms, and a gentamicin protection assay demonstrated an intracellular localization of B. burgdorferi."

    "Cytopathic effects were not observed following infection of these cell lines with B. burgdorferi, and internalized spirochetes were found to be viable."

    "Invasion of neural cells by B. burgdorferi provides a putative mechanism for the organism to avoid the host's immune response while potentially causing functional damage to neural cells during infection of the CNS."

    How can there at least not be a scientific discussion about the notion of persistence when there is evidence Bb can be intracellular? Especially in the brain?

    I do not understand how a number of journalists and denialists about the potential for persistence fail to address these studies. If they are in fact addressing them, please point me to their counterpoints. Thanks.

  2. I think I meant to write, "How can there not be at least a scientific discussion..." Sorry - tired. Hope those reading got the gist.

  3. CO,

    What makes the denialism even more troubling for me is that many theories since 1997 remain either unproven or not acknowledged. Here are a couple of examples (which may span two comments):

    Semin Neurol. 1997 Mar;17(1):57-62.
    Mechanisms of injury in Lyme neuroborreliosis.
    Garcia-Monco JC, Benach JL.
    Department of Neurology, Hospital de Galdacano, Vizcaya, Spain.

    Neurologic injury in infection with Borrelia burgdorferi can be due to the direct action of the spirochetes and spirochetal products on neural cells. There is in vitro evidence for the adherence of this organism to neurons, to glia, and to Schwann cells. Adhesion was found to be associated with galactocerebroside, a glycolipid component of myelin, and could act as a receptor for B. burgdorferi in oligodendroglia and in Schwann cells. Another pathway for neurologic injury could be through amplification of the inflammatory response by newly invading organisms (acute) and persisting (chronic) organisms. There is experimental evidence for production of IL-6, TNF-alpha, and nitric oxide by neural cells exposed to B. burgdorferi. Similar findings have been obtained from neuroborreliosis patients. Although less likely, there is the possibility that autoreactive mechanisms could have a role in the development of some manifestations of neuroborreliosis.

    [PubMed - indexed for MEDLINE]

    Semin Neurol. 1997 Mar;17(1):63-8.

    Immunologic mechanisms in Lyme neuroborreliosis: the potential role of autoimmunity and molecular mimicry.

    Sigal LH.


    Department of Medicine and Disease Center, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick 08903-0019, USA.


    Most of the clinical manifestations of Lyme disease are due to the local presence of the causative agent, Borrelia burgdorferi, in the affected tissues. However, the precise means of tissue damage are not well understood and there is no proof that the organism, live or dead, is always present. An understanding of the complex interaction between the organism, the immune response elicited by the organism, and the host can explain manifestations of the disease and persistence of symptoms and signs after the antibiotic-induced death of the organism. It is possible that dead spirochetes, or fragments thereof may persist and act as a focus of ongoing inflammation. Different immunogenetic types may predispose to different immunologic responses, with distinct clinical outcomes. Vascular changes induced by the infection, either by local infection or the effects of cytokines on the vessel wall, may underlie tissue pathology. Finally, the immune response to B. burgdorferi may elicit the production of antibodies capable of recognizing and damaging or modifying normal host tissues. Only by establishing the mechanisms causing tissue damage in Lyme disease can rational therapeutic strategies be developed. Only by understanding these mechanisms can physicians and patients interpret clinical responses to therapy and accurately appreciate the clinical prognosis.

    PMID: 9166962 [PubMed - indexed for MEDLINE]

  4. Rita,

    Unproven and not acknowledged - or are they taking them in a different direction? I think there is some acknowledgement of them - but the issue is remaining unproven.

    That's a big problem: There are a few hypotheses on the table, but here we are, years later without a definite theory as to what causes persisting symptoms.

    And as I've said before: Maybe the cause isn't the same in every person with such symptoms. This is what makes the issue so complicated.

    Compare the statements within the study abstracts you posted to more recent ones.

    There is an evolution to these studies. What you will notice over time - and in particular, the past 10-12 years - is that a number of them shift away from following basic pathogenesis to what appears to happen in immunological and biochemical response.

    Look at:

    Pathogenesis of Lyme neuroborreliosis: Borrelia burgdorferi lipoproteins induce both proliferation and apoptosis in rhesus monkey astrocytes.
    Ramesh G, Alvarez AL, Roberts ED, Dennis VA, Lasater BL, Alvarez X, Philipp MT. Eur J Immunol. 2003 Sep;33(9):2539-50.

    Brain invasion by Borrelia burgdorferi, the agent of Lyme disease, results in an inflammatory and neurodegenerative disorder called neuroborreliosis. In humans, neuroborreliosis has been correlated with enhanced concentration of glial fibrillary acidic protein in the cerebrospinal fluid, a sign of astrogliosis. Rhesus monkeys infected by us with B. burgdorferi showed evidence of astrogliosis, namely astrocyte proliferation and apoptosis. We formulated the hypothesis that astrogliosis could be caused by spirochetal lipoproteins. We established primary cultures of rhesus monkey astrocytes and stimulated the cells with recombinant lipidated outer surface protein A (L-OspA), a model B. burgdorferi lipoprotein, and tripalmitoyl-S-glyceryl-Cys-Ser-Lys(4)-OH (Pam(3)Cys), a synthetic lipopeptide that mimics the structure of the lipoprotein lipid moiety. L-OspA elicited not only astrocyte proliferation but also apoptosis, two features observed during astrogliosis. Astrocytes produced both IL-6 and TNF-alpha in response to L-OspA and Pam(3)Cys. Proliferation induced by L-OspA was diminished in the presence of an excess of anti-IL-6 antibody, and apoptosis induced by this lipoprotein was completely suppressed with anti-TNF-alpha antibody. Hence, IL-6 contributes to, and TNF-alpha determines, astrocyte proliferation and apoptosis, respectively, as elicited by lipoproteins. Our results provide proof of the principle that spirochetal lipoproteins could be key virulence factors in Lyme neuroborreliosis, and that astrogliosis might contribute to neuroborreliosis pathogenesis.

    Okay, so this is one study from 2003. I'm going to pull two statements out of this:

    "We formulated the hypothesis that astrogliosis could be caused by spirochetal lipoproteins."

    "Proliferation induced by L-OspA was diminished in the presence of an excess of anti-IL-6 antibody, and apoptosis induced by this lipoprotein was completely suppressed with anti-TNF-alpha antibody."

    Notice that the focus is not on where spirochetes are found - brain invasion is already a given. The focus is on lipoproteins and their effect on the immune system.

    Okay, next...

  5. (more for Rita)

    Pathogenesis of Lyme neuroborreliosis: mitogen-activated protein kinases Erk1, Erk2, and p38 in the response of astrocytes to Borrelia burgdorferi lipoproteins.
    Ramesh G, Philipp MT. Neurosci Lett. 2005 Aug 12-19;384(1-2):112-6.

    Lyme borreliosis, which is prevalent both in the US and in Europe, is an infectious disease that may cause local inflammation in numerous organs. We have hypothesized that, as with some neurodegenerative diseases, the pathogenesis of the neurocognitive deficiencies associated with Lyme neuroborreliosis of the central nervous system also has an inflammatory component. Dysregulated production of pro-inflammatory cytokines such as IL-6 and TNF-alpha can lead to neuronal damage. Mitogen-activated protein kinases (MAPK) play a key role in the regulation of neuronal development, growth, and survival, as well as that of pro-inflammatory cytokine production. As a model, we explored the possibility that MAPK-mediated lipoprotein-induced apoptosis and gliosis of rhesus monkey astrocytes stimulated in vitro. Lipoproteins are the key inflammatory molecule type of Borrelia burgdorferi, the spirochete that causes Lyme disease, and we had previously shown that lipoprotein-induced TNF-alpha production in astrocytes caused astrocyte apoptosis, and IL-6 enhanced proliferation of these cells. Lipoproteins readily activated p38 and Erk1/2 MAPK, thus enlisting these pathways among the kinase pathways that spirochetes may address as they invade the central nervous system. We also investigated whether specific inhibition of p38 and Erk1/2 MAPK would inhibit TNF-alpha and IL-6 production and thus astrocyte apoptosis, and proliferation, respectively. Lipoprotein-stimulated IL-6 production was unaffected by the MAPK inhibitors. In contrast, inhibition of both p38 and Erk1/2 significantly diminished TNF-alpha production, and totally abrogated production of this cytokine when both MAPK pathways were inhibited simultaneously. MAPK inhibition thus may be considered as a strategy to control inflammation and apoptosis in Lyme neuroborreliosis.

    I have more to say on this, but I want to hear your thoughts on this first. What do you see happening in these studies?

  6. CO,

    I've tried posting my comment (shortening it each time), but I'm having trouble doing so. My very condensed comment (in case it gets through) is that there is a definite shift in research toward addressing the inflammation that appears to be the root cause of many neurodegenerative, neuropsychiatric, and even autoimmune disorders.

    That's all very well and good, except forgetting about the original trigger -- especially in the case of Lyme disease and other infectious diseases -- doesn't seem like a very good idea to me. It's probably not a question of persistent infection OR immune response, but a combination of those two factors and many more (like innate immunity, environment, genetics, etc).

    I'll try to post my longer comment later or tomorrow.

  7. Another research grant has been awarded to study the effect of tick-borne illnesses on the immune system (rather than the central nervous system as just one example):

    UC Riverside Entomologist to Study Diseases Transmitted by Ticks

    Study by Joao Pedra supported by five-year grant from National Institutes of Health

    (August 4, 2011)

    RIVERSIDE, Calif. – Summer for most people means time spent outdoors, which could also mean increased exposure to bugs and, possibly, arthropod-borne diseases, such as “rickettsial diseases” – infectious diseases spread by bacteria, which, generally, are transmitted by lice, fleas, ticks and mites.

    Now a $1.6 million grant from the National Institutes of Health (NIH) will enable an entomologist at the University of California, Riverside to study how our immune system responds to rickettsial infection.

    The immune system is composed of innate and adaptive immunity. The first line of war against infectious agents is innate immunity, while adaptive immunity acts as a second line of defense and protects us against re-exposure to the same pathogen.

    “If we understand how our innate immune system works during rickettsial infection, we can use this knowledge to devise novel therapeutics that delay or prevent the onset of rickettsial diseases,” said Joao Pedra, the principal investigator of the five-year grant and an assistant professor of entomology.

    CO, I think my sampling of research studies with a clear focus on ways to reduce inflammation -- regardless of the original cause(s) is too long for the comments section, so I'll include this surprising one where even obesity is described as a pro-inflammatory disease. At least one proposed treatment might surprise you and others:

    Annu Rev Nutr. 2010 Aug 21;30:173-99.

    Targeting inflammation-induced obesity and metabolic diseases by curcumin and other nutraceuticals.

    Aggarwal BB.


    Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.


    Extensive research within the past two decades has revealed that obesity, a major risk factor for type 2 diabetes, atherosclerosis, cancer, and other chronic diseases, is a proinflammatory disease. Several spices have been shown to exhibit activity against obesity through antioxidant and anti-inflammatory mechanisms. Among them, curcumin, a yellow pigment derived from the spice turmeric (an essential component of curry powder), has been investigated most extensively as a treatment for obesity and obesity-related metabolic diseases. Curcumin directly interacts with adipocytes, pancreatic cells, hepatic stellate cells, macrophages, and muscle cells. There, it suppresses the proinflammatory transcription factors nuclear factor-kappa B, signal transducer and activators of transcription-3, and Wnt/beta-catenin, and it activates peroxisome proliferator-activated receptor-gamma and Nrf2 cell-signaling pathways, thus leading to the downregulation of adipokines, including tumor necrosis factor, interleukin-6, resistin, leptin, and monocyte chemotactic protein-1, and the upregulation of adiponectin and other gene products. These curcumin-induced alterations reverse insulin resistance, hyperglycemia, hyperlipidemia, and other symptoms linked to obesity. Other structurally homologous nutraceuticals, derived from red chili, cinnamon, cloves, black pepper, and ginger, also exhibit effects against obesity and insulin resistance.

    PMID: 20420526 [PubMed - indexed for MEDLINE] PMCID: PMC3144156 Free PMC Article

  8. Rita,

    It's late, so I'm just going to leave this response for now:


    I do anyway. I like it.

  9. Rita,

    Now that I've slept some and am drinking coffee, I am up to commenting more.

    Yes, you noticed what I have - that the focus is on inflammation in neurodegenerative, neuropsychiatric, and even autoimmune disorders.

    And the concern you stated about forgetting the original trigger is important, because if one treats the patient as if they do not have a persistent infection when they do - all hell can break loose.

    Giving steroids such as Prednisone to patients who are fighting off an infection is like throwing gas on a fire... suppressing the immune system has been a bad idea in anyone who has Lyme disease.

    So if anyone thinks treating individual patients with certain drugs is a good idea, they had better be pretty damn sure that those patients are in fact suffering from conditions for which those drugs are safe and effective.


  10. (For Rita - more)

    But getting back to the original topic - the shift in research from pathogenesis to studying inflammation and immune factors, I'm going to comment on the last abstract I posted above:

    "We have hypothesized that, as with some neurodegenerative diseases, the pathogenesis of the neurocognitive deficiencies associated with Lyme neuroborreliosis of the central nervous system also has an inflammatory component."

    "Dysregulated production of pro-inflammatory cytokines such as IL-6 and TNF-alpha can lead to neuronal damage."

    "As a model, we explored the possibility that MAPK-mediated lipoprotein-induced apoptosis and gliosis of rhesus monkey astrocytes stimulated in vitro."

    So, when I read something like this, and compare it to earlier research that parts of the Lyme patient community tends to mention - it becomes clearer to me that a number of researchers have been focusing more on the brain's and immune system's response to Borrelia burgdorferi and less to pathogenesis and morphological changes. These brain studies are only two such examples - there are more - I just picked two of the more dramatic ones.

    So anyone reading a lot more of this kind of research in the past decade or so is going to be focusing more on the immune or autoimmune factors related to Lyme disease - and less on what the spirochetes are doing, because this is where a lot of the research has been.

    There are different lenses through which to view the disease process - that much is clear to me. And I think that looking at where Bb goes and what it does in vivo is important. That knowledge is something I want and everyone in the Lyme patient community wants because it could give us insight into how to better treat this formidable foe.

    From the perspective of those doing this research, some of them already may be thinking that more antibiotics are not the solution - and maybe not because they are antibiotics - but because they're the wrong antibiotics for the job and we don't have new ones. Or maybe because an entirely new kind of treatment is needed for neuroborreliosis that is of short duration and effective - and we don't have one yet.

    The goal for some of these researchers may not be to kill every last spirochete but to find drugs which help the immune system overcome their effect (and maybe by extension, the last few spirochetes will die off).

    Here is a key phrase from the above abstract:

    "MAPK inhibition thus may be considered as a strategy to control inflammation and apoptosis in Lyme neuroborreliosis."

    They think MAPK inhibition may control inflammation and apoptosis - which is cell death - in Lyme neuroborreliosis. So maybe here they were thinking about the possibility of developing some sort of MAPK inhibitor drug and not antibiotics to treat neuroborreliosis. Maybe yes, maybe no and they discarded the idea.

    This is where things get tricky, of course:

    Wouldn't you want to kill every last Bb in your body? Wouldn't you be afraid of the few remaining ones slowly reproducing and gaining in population and migrating to who knows where?

    I think most people would be, and this is why the idea of a MAPK inhibitor instead of antibiotics sounds, well, offbase to many. That it's not addressing the source of the problem and it's just another drug that helps with symptoms but doesn't cure infection.

    So naturally there are issues with this approach, and concern that any non-antimicrobial treatment won't get at the source and may even make matters worse.

    Which is why, I think, one has to be very careful to define the source or sources of the problem. Not only as a researcher for other researchers - but as a researcher whose work is going to be reviewed by the public and patients who are seeking answers.

  11. Rita,

    For your consideration, since you were looking at the possibility of both presence of infection and immune factors as a cause of persisting symptoms:

    The paradox of matrix metalloproteinases in infectious disease
    P. T. G. Elkington, C. M. O'Kane, J. S. Friedland
    Clinical & Experimental Immunology. Volume 142, Issue 1, pages 12–20, October 2005.

    From the full text:

    "Successful eradication of infection by the host requires the influx of effector cells, killing of the pathogen, resolution of inflammation and finally remodelling of the extracellular matrix (ECM). Host-derived matrix metalloproteinases (MMPs) are necessary for the successful execution of these events. However, excessive inflammation following infection may cause tissue damage and MMPs are implicated in causing this immunopathology. Tissue destruction may favour pathogen dissemination or persistence, by breaking down barriers to spread or by creating an immunoprivileged site that is poorly accessed by host immune cells. Here we will overview the role of MMPs in the normal immune response and then consider how MMPs may contribute to infection-related pathology."

    So here's one example of how triggers of a typical process can lead to post-infectious tissue damage and also infection dissemination and persistence. There are other processes which are implicated in persistence, too.

    On another more philosophical note:

    In terms of how to better treat persisting symptoms of Lyme disease and some coinfections, the treatment may be something outside the box in terms of what many patients may be thinking - that it has to be either antibiotics or steroids involved. Coming up with solutions from only those two boxes limits innovation and the ability to find what may be the best treatment.

    It's possible that the future contains neither as a treatment, and solutions will be something different - such as the use of protease inhibitors to cure Chagas disease in mice. (By the way, to anyone reading this: This is not a suggestion that you go out and try any old protease inhibitors to treat your own tickborne infections - the drugs have to be specifically designed for specific conditions.)

  12. CO,

    I've just lost another long comment to cyberspace, so I think I'll try breaking it up into smaller ones (at the risk of losing my train of thought).

    In response to your question (in bold):

    Wouldn't you want to kill every last Bb in your body? Wouldn't you be afraid of the few remaining ones slowly reproducing and gaining in population and migrating to who knows where?

    my answer would be a resounding yes, however this applies to more than a Bb infection.

    I'm not sure why anyone would doubt the possible activation or reactivation of a seemingly "dormant" or "latent" or "remnants-only" of any infection given the right (i.e. adverse) conditions. I'll start with this one, and then post a more personal comment. Note that that I am providing the link for reference only -- not required or even recommended reading:

    Excluding the possibility of tuberculosis is a common clinical situation. Older patients, chronic lung disease and increased use of immunosuppression increase the risk of tuberculosis reactivation and have created an increasingly common scenario where active contagious tuberculosis needs to be excluded quickly and with minimum inconvenience.

    (to be continued)

  13. To continue ...

    I have often wondered about my husband's situation when it comes to possible reactivation of infections(s) and the consequences of prolonged immunosuppressive therapy.

    My husband had severe asthma as a child. He eventually "outgrew" that and showed no signs of this by in early adulthood. After a mysterious infection (I am deliberately not speculating about this in public) and a move from Montreal to Toronto (where pollution was much worse at the time), my husband's childhood asthma was reactivated and required prolonged treatment with Prednisone to save his life (which he nearly lost in the ER more than once). Each time he was tapered off the Prednisone, his breathing took a turn for the worse, so the logical thing to do was keep him on steroids despite the known long-term consequences of doing so. Eventually, over the course of many years and new and improved inhalers, he was able to wean off the Prednisone.

    Each time my husband developed so much as a cold, he ended up requiring Prednisone, and I don't doubt this contributed to him then developing an obvious chest infection that required heavy-duty antibiotic treatment. It seemed like a bit of a vicious cycle.

    After some non-chest recurring infections that required Biaxin and Cipro (separately) for a month at a time (as prescribed by my husband's urologist), things seemed to improve and they are mostly stable now. Each and every respiratory infection (viral or not to begin with) does still result in yet another course of prednisone and (not surprisingly) antibiotics.

    I pointed this out to my husband, and asked him to try not dosing himself with prednisone in anticipation of days with high pollution rates (a habit his family physician endorsed but I wasn't fully aware of). Not only is my husband less edgy (a consequence of steroid use), the number of "colds" he experiences has been reduced. There is speculation (I'm not sure about proof) that the cleaner air we've been experiencing in Toronto is the direct result of manufacturing plants in the U.S. being closed in the past few years, so this is another (environmental) factor that may be contributing to my husband's generally-improved health.

    That's why I tend to view simplistic answers to complex problems with a great deal of skepticism. Most healthcare providers seem to think that prescribing inhalers even to school-aged children is the "answer" to dealing with increasing rates of asthma. I beg to differ -- wondering why so many people are developing asthma and other allergic and/or autoimmune disorders in the first place.

    Okay ... I need a brain break.

  14. CO,

    Okay, so what was my point in telling you my husband's story? Simply put, I believe that immunosuppressants may be necessary at times for symptom relief and even to save lives. On the other hand, the suppression of one's immune system does contribute to opportunistic infections and possibly even the reactivation of infections (think TB) that were thought to be eliminated in the past.

    For at least some people with asthma (and no doubt other health conditions), treatment with immunosuppressives may provide temporary relief -- but at a very high price which may not manifest for many years. Our dentist told my husband years ago that countless patients were mystified by their teeth starting to break or fall out for no apparent reason. "Do you use Prednisone?" is his first question, and the answer is almost always "yes".

    Int Arch Allergy Immunol. 2003 Nov;132(3):210-4.

    Asthma as a paradigm for autoimmune disease.

    Rottem M, Shoenfeld Y.


    Division of Allergy, Asthma and Immunology, HaEmek Medical Center, Afula, Israel.


    Allergy and autoimmunity result from dysregulation of the immune system. Until recently, it was generally accepted that the mechanisms that govern these disease processes are quite disparate; however, new discoveries suggest possible common pathogenetic effector pathways. This review illustrates the concomitant presentation of these conditions and the potential relationship or common mechanisms in some cases, by looking at the key elements that regulate the immune response in both asthma and autoimmune conditions: mast cells, antibodies, T cells, cytokines, and genetic determinants. The parallel appearance of asthma and autoimmune conditions in the same patients may reveal that such aberrations of the immune system have a common pathophysiologic mechanism. Mast cells, which play a key role in asthma, and the wealth of inflammatory mediators they express, make it likely that they have profound effects on many autoimmune processes. Activation of protein kinases by inflammatory cytokines and environmental stresses may contribute to both allergic and autoimmune diseases. The presence of autoantibodies in some allergic diseases suggests an autoimmune basis for these conditions. Because of the central role T cells play in immune reactivity, the T cell receptor loci have long been considered important candidates for a common disease susceptibility within the immune system such as asthma, atopy, and autoimmunity. Immunomodulation is the key to successful treatment of asthma and autoimmune conditions.

    Copyright 2003 S. Karger AG, Basel

    PMID: 14646381 [PubMed - indexed for MEDLINE]

    Perhaps immune "modulating" treatments that satisfy the need to tame an overactive immune system without compromising a person's ability to fight infections is the answer. Easy for me to say -- not so easy to create.

  15. Rita wrote, "Perhaps immune "modulating" treatments that satisfy the need to tame an overactive immune system without compromising a person's ability to fight infections is the answer. Easy for me to say -- not so easy to create."

    I think this is where the research is at and has been for some time... but how long it will take to move a clinical idea to actual patients? Who knows?

    It's also clear that immune suppressing drugs are suboptimal for so many people - but in some cases are required, such as anti-rejection drugs for those with organ transplants. That might change, though, with the use of bone marrow transplants.

    I see immunology as a very hot field right now. There is so much to learn. I just wish discoveries became useful applicable changes in medicine faster than they are in order to save and improve lives.

  16. Rita,

    Wanted to add here that I am sorry about your husband's health problems and hope he is doing better in Toronto (sounds like it). I have been on prednisone for short periods in the past, pre-Lyme, and I did not like the side effects either. Bad insomnia, elevated temperature, and irritability are what I recall - but it's been years.

  17. Thanks, CO. My husband really is doing quite well these days, and the most dramatic and sustained improvement came about after starting his twice-daily use of Symbicort (Budesonide/Formoterol) - an inhaler. According to Wiki, he could do worse:

    "Budesonide in comparison with prednisolone has been associated with fewer bone density losses, and, unlike other corticosteroids, has little influence on the hypothalamic-pituitary-adrenal axis, which also limits the need of tapering before discontinuation. Overall, it has a lower incidence of systemic manifestations than similar medications".

    My husband's family doctor says her patients either notice a dramatic improvement or Symbicort doesn't seem to help at all -- underlining the theory that no two humans should be expected to respond to any specific therapy in exactly the same way. A lot of medicine remains trial and error.

    I just remembered that the emerging field of psychoneuroimmunology may be at least partially responsible for the shift in research direction that we've both been noticing. After taking a look at this site (and particularly the meeting held in June 2011), there is certainly an attempt to link infectious diseases, immunity, stress and other factors when it comes to understanding disease processes.

    Thanks for the link regarding bone marrow transplants. I had read about that with great interest a while back -- mostly because I worked for a short time as a Transplant Coordinator in the Nephrology department at Toronto's Hospital for Sick Children. I was responsible for the IT end and maintaining the transplant list, and this required attending daily meetings to review the status of our young patients waiting for their first or sometimes second transplant. I got to know the patients and their parents quite well despite my mostly technical responsibilities because my office was on the same floor as the inpatient and dialysis units. It was a dream job for me until I realized the infrastructure to support the type of networking changes needed simply wasn't there and wouldn't be in the foreseeable future. Once I started feeling like a glorified list keeper rather than an instrument of the changes that everyone hoped could be implemented in short order, I knew it was time to move on. It was still a great experience and working environment. I have worked at three hospitals in my lifetime (one in Montreal and two in Toronto), and Sick Kids was my favourite by far. Our healthcare system in Canada isn't perfect by any means, but I do know how dedicated some people really are to their work. As a patient, I've also met people who either made a poor career choice to begin with or who ought to move on.

    Okay, so much for my social commentary. The transplant article brought back a lot of memories (mostly good ones).


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