posted
Carrying such infections are we immune compromised?
All the major bacterias and viruses state if we are immune compromised it can be difficult to rid....i don't have cancer or HIV but can i say having lyme and co infections i am in danger too?
-------------------- May God Bless you, answer your prayers, relieve you of your pain and make you stronger than what you are today. Ameen. Posts: 341 | From Columbia, MD | Registered: Jan 2009
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Keebler
Honored Contributor (25K+ posts)
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- Absolutely, those dealing with chronic borrelia & other tick borne infections are immune compromised.
[One major reason not to get any vaccines - in addition to the additives that can have much worse of an effect on those with lyme.]
In "danger"? Well, with chronic / persistent lyme (and the coinfections that go with it) there is not much worse.
The "danger" of catching this or that flu is not really too much of a worry, though. I'll try to explain why I see it that way.
1. No point in worrying anyway. If we know our health / our immunity (our ability to manage anything else on our plate) is an issue we just take the best care we can of ourselves and hope not to catch the current flu.
As for food borne pathogens, extra vigilance is required but I think most are just not aware of the steps all should be taking in this area, anyway.
2. With lyme, most often immune function is "flipped" - part is just so overworked trying to find evasive microbes. Another part is just too worn out to do much.
Still, we do the best we can with particular support methods, avoid things that could be a load. If we do get hit with a flu or whatever, we just employ the best techniques we have to take care of ourselves.
For some, they don't catch colds for long periods of time but, for others, they sure can. There is no fabulous freebie on that part.
Caution: do NOT attempt to "boost" immune function. That can be a disaster if the body is pushed when it's already just so stressed. SUPPORT is the key.
As for terms, some who have the idea of support firmly in mind might use the term "boost" so it's a bit tricky to determine until really looking into methods / ingredients, etc.
Just do not push any body organ or system. It's all about modulation, support. Gentle, consistent, assertive but not aggressive. -
Posts: 48021 | From Tree House | Registered: Jul 2007
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Keebler
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Articles / Books / Herbal Safety considerations & reference books; etc. -
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Keebler
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posted
- SLEEP matters tremendously for immune support. If that is elusive, then "healthy assertive resting" skills are so much more important.
Gather an "urgent care" support kit of sorts. ELDERBERRY EXTRACT is a good start. -
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Brussels
Frequent Contributor (5K+ posts)
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posted
Kleeber is absolutely right. We are all immune compromised, and that is THE REASON why we fell sick with chronic infections. It was not the tick bite.
I'm still immuno compromised, but tick bites make us less sick than before. Before, just one bite meant hell. Now, we still get bitten, but infection can be controlled.
Posts: 6199 | From Brussels | Registered: Oct 2007
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Lymedin2010
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posted
19 studies revealing immunosuppression from Lyme disease.
1994 Feb - Antigens of Lyme disease of spirochaete Borrelia burgdorferi inhibits antigen or mitogen-induced lymphocyte proliferation. "These results have demonstrated an immune suppressive mechanism of B. burgdorferi. The magnitude of host immune responses may be dependent on the degree of suppression which is related to the spirochaete quantity and their length of presence in the host." http://www.ncbi.nlm.nih.gov/pubmed/8173554
1997 Jul - Why is chronic Lyme borreliosis chronic? "Recent findings indicate that the most important cell for antigen presentation, the epidermal Langerhans cell (LC), is invaded by B. burgdorferi in early Lyme borreliosis. Therefore, LCs were stained immunohistochemically with different markers to investigate their functional activity. Numbers of CD1a+ LCs were reduced in erythema migrans but normal or slightly elevated in ACA. In both diseases there was also a marked downregulation of major histocompatibility complex class II molecules on LCs, as measured by staining of human leukocyte antigen DR. This phenomenon might be a mechanism that protects against the presentation of autoantigens and may be the cause of the impaired capacity of LCs to eliminate B. burgdorferi antigens, thus explaining why CLB is chronic." http://www.ncbi.nlm.nih.gov/pubmed/9233667
1998 Jun - Borrelia burgdorferi Stimulates the Production of Interleukin-10 in Peripheral Blood Mononuclear Cells from Uninfected Humans and Rhesus Monkeys "These results demonstrate that B. burgdorferi can stimulate the production of an antiinflammatory, immunosuppressive cytokine in naive cells and suggest that IL-10 may play a role both in avoidance by the spirochete of deleterious immune responses and in limiting the inflammation that the spirochete is able to induce." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC108257
2000 Jul - Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA). Gary Wormser, lead author of the Lyme disease guideline opinions is admitting OspA, the antigen in the Lyme vaccine and a surface protein, induces immunosuppression in a canine model of Lyme disease. "...OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression. ... Future studies designed to delete the particular region or component of the OspA molecule responsible for this effect may lead to improved vaccine preparations."
NOTES: lymphocytes - immune system white blood cells. cell cycle phase progression - replication.
2000 Dec - Early induction of gamma interferon and interleukin-10 production in draining lymph nodes from mice infected with Borrelia burgdorferi. "The differential effect of IL-10 on IFN-gamma production in C57BL/6J and C3H/HeJ mice suggests that IL-10 is probably involved in the regulation of IFN-gamma production by LN cells during infection and may be at the root of the differential susceptibility to Lyme arthritis in these two strains of mice." http://www.ncbi.nlm.nih.gov/pubmed/11083848
2003 Jul - Borrelia burgdorferi-induced tolerance as a model of persistence via immunosuppression. Summary "...we characterized tolerance induced by B. burgdorferi, describing a model of desensitization which might mirror the immunosuppression recently attributed to the persistence of Borrelia in immunocompetent hosts." http://www.ncbi.nlm.nih.gov/pubmed/12819085
2003 Sep - Interaction of Borrelia burgdorferi sensu lato with Epstein-Barr virus in lymphoblastoid cells. "Since the possibility of interruption of latent Epstein-Barr virus infection has been suggested by the induction of the lytic virus cycle with chemical substances, other viruses, and by immunosuppression, we hypothesized that the same effect might happen in B. burgdorferi sensu lato infection as happens in Lyme disease patients with positive serology for both agents. ... Demonstration of such findings must be interpreted cautiously, but may prove a mixed borrelial and viral cause of severe neurological disease." http://www.ncbi.nlm.nih.gov/pubmed/12630667
2006 Mar 15 - Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes. "We show that stimulation of human monocytes with B. burgdorferi lysate, lipidated outer surface protein A, and triacylated lipopeptide Pam3CysSerLys4 results in the up-regulation of both TLR2 and TLR1 but the down-regulation of TLR5, the receptor for bacterial flagellin, and that this effect is mediated via TLR2. ... In addition, TLR2 stimulation rendered cells hyporesponsive to a TLR5 agonist. ..." http://www.ncbi.nlm.nih.gov/pubmed/16479520
2006 Jun - Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression. IMPORTANT: The difference in HLAs cause the two types of Lyme. The hyperimmune outcome, and immunosuppressed outcome. Dr Alan Steere completely denied the existence of the immunosuppressed outcome by deliberately designing the Lyme two-tier test so the neurological outcome would test negative. Those patients are sent off to psychiatrists and told they are crazy. "These results show that signaling through TLR1/2 in response to B. burgdorferi can elicit opposite immunoregulatory effects in blood and in brain immune cells, which could play a role in the different susceptibility of these compartments to infection." http://www.ncbi.nlm.nih.gov/pubmed/16783164
2006 Oct - Interleukin-10 anti-inflammatory response to Borrelia burgdorferi, the agent of Lyme disease: a possible role for suppressors of cytokine signaling 1 and 3. "... Because it is known that cytokine signaling are induced by IL-10 and that B. burgdorferi and its lipoproteins most likely interact via TLR2 or the heterodimers TLR2/1 and/or TLR2/6, we hypothesized that cytokine signaling are induced by IL-10 and B. burgdorferi and its lipoproteins in macrophages and that cytokine signaling may mediate the inhibition by IL-10 of concomitantly elicited cytokines. We report here that mouse J774 macrophages incubated with IL-10 and added B. burgdorferi spirochetes (freeze-thawed, live, or sonicated) or lipidated outer surface protein A (L-OspA) augmented their SOCS1/SOCS3 mRNA and protein expression, with SOCS3 being more abundant. Pam(3)Cys, a synthetic lipopeptide, also induced SOCS1/SOCS3 expression under these conditions, but unlipidated OspA was ineffective..." http://www.ncbi.nlm.nih.gov/pubmed/16988256
2007 Jan - Decreased up-regulation of the interleukin-12Rbeta2-chain and interferon-gamma secretion and increased number of forkhead box P3-expressing cells in patients with a history of chronic Lyme borreliosis compared with asymptomatic Borrelia-exposed individuals. "... In addition, regulatory T cells might also play a role, by immunosuppression, in the development of chronic Lyme borreliosis." http://www.ncbi.nlm.nih.gov/pubmed/17177959
2008 Mar - Viable Borrelia burgdorferi Enhances Interleukin-10 Production and Suppresses Activation of Murine Macrophages "B. burgdorferi induces IL-10 in vivo ... Together, these results suggest that viable B. burgdorferi can suppress early primary macrophages Mφ responses during infection by causing increased release of IL-10." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2258815
2010 - Our experience with examination of antibodies against antigens of Borrelia burgdorferi in patients with suspected lyme disease. "RESULTS: All patients had specific antiborrelial antibodies confirmed by using the westernblot in spite of negative ELISA. Immunological investigations revealed a deficiency of cellular immunity in all patients and in a part of them (15.6%) a deficiency of humoral immunity was also found. The presence of different types of autoantibodies was detected in 17 (53.1%) patients. CONCLUSION: In patients with persisting difficulties that could be associated with Lyme disease, it is necessary to use the westernblot test which could prove the presence of specific antibodies. It is probably due to the very low production of specific antibodies caused also by the status of immune deficiency detected in all our patients (Tab. 1, Ref. 11)." http://www.ncbi.nlm.nih.gov/pubmed/20437826
2011 May 26 - PLOS Pathogens: Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation "Together, these findings suggest a novel evasion strategy for B. burgdorferi: subversion of the quality of a strongly induced, potentially protective borrelia-specific antibody response via B. burdorferi's accumulation in lymph nodes." http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1002066
2011 Dec - Interleukin-10 alters effector functions of multiple genes induced by Borrelia burgdorferi in macrophages to regulate Lyme disease inflammation. "Our data show that IL-10 alters effectors induced by B. burgdorferi in macrophages to control concomitantly elicited inflammatory responses. Moreover, for the first time, this study provides global insight into potential mechanisms used by IL-10 to control Lyme disease inflammation." http://www.ncbi.nlm.nih.gov/pubmed/21947773
2012 Feb 1 - TLR2 signaling depletes IRAK1 and inhibits induction of type I IFN by TLR7/9. "The inhibitory effect of TLR2 was not dependent on new protein synthesis or intercellular signaling. IL-1R-associated kinase 1 (IRAK1) was depleted rapidly (within 10 min) by TLR2 agonist, but not until later (e.g., 2 h) by TLR9 agonist. Because IRAK1 is required for TLR7/9-induced IFN-I production, we propose that TLR2 signaling induces rapid depletion of IRAK1, which impairs IFN-I induction by TLR7/9. This novel mechanism, whereby TLR2 inhibits IFN-I induction by TLR7/9, may shape immune responses to microbes that express ligands for both TLR2 and TLR7/TLR9, or responses to bacteria/virus coinfection." http://www.ncbi.nlm.nih.gov/pubmed/22227568
2012 Oct - Different patterns of expression and of IL-10 modulation of inflammatory mediators from macrophages of Lyme disease-resistant and -susceptible mice. "Neutralization of endogenously produced IL-10 increased production of inflammatory mediators, notably by macrophages of C57 mice, which also displayed more IL-10 than C3H macrophages. The distinct patterns of pro-inflammatory mediator production, along with TLR2/TLR1 expression, and regulation in macrophages from Lyme disease-resistant and -susceptible mice suggests itself as a blueprint to further investigate differential pathogenesis of Lyme disease." http://www.ncbi.nlm.nih.gov/pubmed/23024745
2013 Dec 19 - Borrelia burgdorferi Elicited-IL-10 Suppresses the Production of Inflammatory Mediators, Phagocytosis, and Expression of Co-Stimulatory Receptors by Murine Macrophages and/or Dendritic Cells "... The IL-10 levels appear able to block many of the immune functions of these anaphase-promoting complexes(needed for cell replication - JS) that should be critical for controlling Bb infection. ... Because macrophages(removes dead/dying cells and dibris - JS) and dendritic(skin-JS) cells are believed to be largely responsible for moderating the early immune responses against Bb deposited into the skin, these findings suggest this IL-10 elicitation may be largely responsible for the dysregulated early leukocyte responses and delayed adaptive responses that are believed to have a major influence in the ability of Bb to efficiently disseminate and persist ... " http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3868605
2015 July 2 - PLOS Pathogens: Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection The Lyme disease bacteria suppresses the immune system. Immunosuppression is one of the worst kinds of damage one can get from an infectious disease. Eventually you contract other infections and they become active for years and decades. Infections like EBV, other herpesviruses, and mycoplasma infections slowly deplete, exhaust, and damage your entire body and mind. "This data illustrate the potent, if temporal, immune suppression induced by Borrelia-infection. Collectively, the data reveal a new mechanism by which B. burgdorferi subverts the adaptive immune response." http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004976
"All the abused patient groups in medicine share what is essentially the same disease. Immune suppression with active opportunistic chronic infections. Lyme disease(OspA damage) , ME/CFS, Gulf War illness (fungal contamination from expired vaccines), Fibromyalgia, Fungal infections, post sepsis syndrome, Gardasil vaccine victims with severe fatigue, and fungal contaminated vaccines.
These websites contain information about the crime;"
posted
So does this mean that we are in danger to get other serious infections/diseases. Same for a patient whose who has HIV for example?
-------------------- May God Bless you, answer your prayers, relieve you of your pain and make you stronger than what you are today. Ameen. Posts: 341 | From Columbia, MD | Registered: Jan 2009
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Keebler
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- sonee,
Yes. But then we also have more tools to prevent and treat since having lyme opens us up to so many ways to care for, support and treat ourselves when other things occur. -
Posts: 48021 | From Tree House | Registered: Jul 2007
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randibear
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oh my yes....
-------------------- do not look back when the only course is forward Posts: 12262 | From texas | Registered: Mar 2007
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Brussels
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posted
I don't think lyme is like HIV AIDS. It is ALSO immunosuppressive, but you can treat lyme and get to remission (meaning, you get to have all borrelia dormant, causing absolutely NO SYMPTOMS).
It means, you may STOP TREATING it, not taking anything against borrelia (since it got dormant).
I do not think the prospect for AIDS patients is the same. I guess, the AIDS patient has to treat for the rest of his / her life, mostly.
And even very rich people die of AIDS, while lyme kills mostly by suicides (when the sufferer can't stand living in misery anymore).
Candida is also immuno suppressive. Epstein Barr virus too. There are quite many things that are immunosuppressive.
Even having liver detox pathways blocked or not working properly has immuno suppressive action.
Smoking, sugar and alcohol have also immuno suppressive action.
Don't worry about the term immuno supression.
Just treat yourself the best you can. Kill, clean, modulate, build your body, control diet.
Posts: 6199 | From Brussels | Registered: Oct 2007
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