Guest guest Posted August 23, 2005 Report Share Posted August 23, 2005 Looking at your post, it seems this one might interest you. I dont know what to make of it tho: ================================= Immunology. 2002 Sep;107(1):46-55. Related Articles, Links Cytokines in Lyme borreliosis: lack of early tumour necrosis factor- alpha and transforming growth factor-beta1 responses are associated with chronic neuroborreliosis. Widhe M, Grusell M, Ekerfelt C, Vrethem M, Forsberg P, Ernerudh J. Division of Clinical Immunology, Faculty of Health Sciences, University of Linkoping, Sweden. mona.widhe@... The clinical outcome of the tick born infection Lyme borreliosis seems to be influenced by the type of immune response mounted during the disease, as suggested by various animal models. Here we report the serum and cerebrospinal fluid levels of tumour necrosis factor- alpha (TNF-alpha), transforming growth factor beta1 (TGF-beta1) and interleukin-6 (IL-6) in samples drawn at different disease intervals during the course of non-chronic neuroborreliosis (n=10), chronic neuroborreliosis (n=15), erythema migrans (n=8, serum only) and controls (n=7). When comparing early neuroborreliosis cerebrospinal fluid samples, significantly higher levels of TNF-alpha were found in non-chronic patients than in chronic patients (P<0.05). Moreover, TGF-beta1 was increased in the early serum samples of non-chronic patients, as compared to chronic patients (P<0.01). Elevated serum levels of TGF-beta1 were also found in erythema migrans as compared to neuroborreliosis and controls (P<0.05). The high TNF-alpha levels noted in early cerebrospinal fluid samples of non-chronic patients only, possibly reflects an ongoing pro-inflammatory immune response in the central nervous system, which could be beneficial in eliminating disease. High serum levels of TGF-beta1 probably mirror an anti-inflammatory response, which might play a role in controlling the systemic immune response. PMID: 12225362 [PubMed - indexed for MEDLINE] > I read the first paper, and the follow-up. These are tentative, > first read responses: > > 1) It seems odd, and very frustrating, that we are told nothing > about the duration of disease, prior treatment history, coinfection > test results, or current clnical presentation in these patients > whose monocytes were assessed for cytokine release. Yet all patients > were from one GP's practice! How hard could it have been to compile > that data? > > Without such information, we have nothing to correlate these > findings to but the selection criteria, which appear to have been > that patients were making enough Bb antibodies to test positive via > serology. > > 2) There is at least one study I recall clearly that shows what at a > glance seems like the inverse result. Immune cells (identified as > macrohpages, not monocytes) exposed to borrelia outer surface > proteins in that study were seen to produce high levels of IL-12, > low levels of IL-10, in a ratio extreme enough to force naive T > cells (Th0) into the Th1 phenotype. The hypothesis considered there > was that by generating this response, borrelial OSPs protected the > bugs from effective antibody development, which they stated required > the presence of Th2 cells. > > 3) I suppose in a very speculative way you could reconcile the > results by saying that the positive antibody status of the 'late > stage' patients acrued from the higher levels of IL-10 facilitating > Th2 cell, antibody-forming responses vs. the inflammmatory response > observed in response to borrelial OSPs in the other study I am > referring to. > > 4) You could end up with a forking immune response that looks a > little like this: > > In response pattern 1, high levels of inflammatory cytokines are > generated but effective antibody development is minimized. Any bugs > that are killed are quickly removed from the body, but not many are. > > In response pattern 2, low levels of inflammatory cytokines are > generated, but effective antibody development is increased. More > bugs are killed, but the inflammatory process needed to get the > lysed bugs and their toxins out of the body are indequate, allowing > these to accumulate. > > In the first response pattern, the immune system would play a > prominent role in generating symptoms, but a minor role in directly > attacking the bugs. > > In the second response pattern, the immune system would play a much > reduced role in generating symptoms, a more significant role in > attacking the bugs. The disease would actually be progressing away > from, not toward, an 'autoimmune' model (though based on the broad > reduction in cytokine release to ANY flavor of LPS, possibly toward > a model of immune deficit). > > One might expect the first hypothesized pattern to correspond more > to arthralgias, the second to correspond more to central and > peripheral nervous system disease. > > It's just a bunch of wild speculation on my part. What a shame that > we know nothing about the actual health status of those patients > whose monocytes were studied. > > I would almost think it worth corresponding with the authors to see > if anything more can be learned. > > S. Quote Link to comment Share on other sites More sharing options...
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