effect of UV irradiation on infection of mice with Borrelia burgdorferi, The Photochemistry and Photobiology, May 2001 by Brown, Eric L, Ullrich, Stephen E, Pride, Michael, Kripke, Margaret L The Effect of UV Irradiation on Infection of Mice with Borrelia burgdorferi(para)
ABSTRACT
These studies addressed the hypothesis that UV radiation (UVR) could affect immune responses in mice infected with Borrelia burgdorferi. Immunity against the Lyme spirochete B. burgdorferi was studied in a marine model of UV-induced immune suppression. Borrelia-specific cellular and humoral responses were examined following immunosuppressive doses of UVR. Low-passage Borrelia were injected intradermally at the base of the tail following irradiation. At various time points after infection the blood was cultured for the presence of Borrelia and the serum analyzed for Borrelia-specific antibodies. Two weeks after infection one hind-limb joint was cultured for the presence of spirochetes and the contralateral joint was examined histologically for arthritis formation. The results demonstrated that UV irradiation, administered at the site of infection or at a distant site, suppressed Borrelia-specific cellular and humoral responses in infected mice. Suppression of delayed-type hypersensitivity and antibody responses to UV was abrogated by administration of anti-interleukin (IL)-10 after UV irradiation. In addition, UV irradiation altered the dissemination pattern of the bacteria from the skin into the blood and exacerbated arthritis when compared with unirradiated controls. From these studies we concluded that UV irradiation can modulate the immune response to Borrelia and exacerbate the subsequent arthritic component of Lyme disease in mice. Furthermore, our studies suggest that IL-10 is in part responsible for the suppression of both cellular and humoral responses in addition to playing a role in the development of Lyme arthritis.
(Abbreviations: APC, antigen-presenting cells; BAT2.2, Borreliaactivated T cells; Bb, Borrelia burgdorferi; BSK II, BarbourStoenner-Kelly; CHS, contact hypersensitivity; DTH, delayedtype hypersensitivity; ELISA, enzyme-linked immunosorbent assay; iBb, inactive Borrelia burgdorferi; i.d., intradermally; IFN, interferon; IL, interleukin; i.p., intraperitoneally; LD, Lyme disease; NRT, normal T cells; PBS, phosphate-buffered saline; SE, standard error; Th, T helper lymphocyte; TNF, tumor necrosis factor; UV-B, ultraviolet B (280-320 nm); UVR, UV radiation.
Posts: 1184 | From north america | Registered: Feb 2003
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-------------------- --Lymetutu-- Opinions, not medical advice! Posts: 96239 | From Texas | Registered: Feb 2001
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WildCondor
Unregistered
posted
Nice...so we all need an Rx to go to the Caribbean...open up a Lyme resort... The sun and the sea always made me feel better! Cool info, thanks!
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klutzo
Frequent Contributor (1K+ posts)
Member # 5701
posted
Sun always makes me feel better too, though I know the folks who promote the Marshall Protocol would say it is ultimately making me feel worse.
I must have a very bad case of Lyme brain this morning, becasue I read this three times and came up with the opposite conclusion.
It looks to me like this study concluded that the sun exposure made the Immune system less able to respond to the Bb, especially in terms of Lyme arthritis. I guess I can't understand research anymore, and it's very sad to keep losing brain function like this.
Klutzo
Posts: 1269 | From Clearwater, Florida, USA | Registered: May 2004
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treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
The one thing our bodies need for any infection is vitamin d.And that comes from the sun.But there are different versions of the socalled V D.
Vitamin D (also known as calciferol) is a hormone precursor that contributes to the maintenance of normal levels of calcium and phosphorus in the blood. Vitamin D is not a true vitamin since human skin can create vitamin D in some circumstance; it may be better described as a conditional vitamin.
Department of Biochemistry, University of Wisconsin-Madison 53706, USA.
Recently, it has been clearly demonstrated that exogenous 1,25-dihydroxyvitamin D3, the hormonal form of vitamin D3, can completely prevent experimental autoimmune encephalomyelitis (EAE), a widely accepted mouse model of human multiple sclerosis (MS). This finding has focused attention on the possible relationship of this disease to vitamin D. Although genetic traits certainly contribute to MS susceptibility, an environmental factor is also clearly involved.Me here spirochetes??coccoid forms in spinal fluid.
It is our hypothesis that one crucial environmental factor is the degree of sunlight exposure catalyzing the production of vitamin D3 in skin, and, further, that the hormonal form of vitamin D3 is a selective immune system regulator inhibiting this autoimmune disease.
Thus, under low-sunlight conditions, insufficient vitamin D3 is produced, limiting production of 1,25-dihydroxyvitamin D3, providing a risk for MS.
Although the evidence that vitamin D3 is a protective environmental factor against MS is circumstantial, it is compelling. This theory can explain the striking geographic distribution of MS, which is nearly zero in equatorial regions and increases dramatically with latitude in both hemispheres.
It can also explain two peculiar geographic anomalies, one in Switzerland with high MS rates at low altitudes and low MS rates at high altitudes, and one in Norway with a high MS prevalence inland and a lower MS prevalence along the coast.
Ultraviolet (UV) light intensity is higher at high altitudes, resulting in a greater vitamin D3 synthetic rate, thereby accounting for low MS rates at higher altitudes. On the Norwegian coast, fish is consumed at high rates and fish oils are rich in vitamin D3.
Further, experimental work on EAE provides strong support for the importance of vitamin D3 in reducing the risk and susceptibility for MS. If this hypothesis is correct, then 1,25-dihydroxyvitamin D3 or its analogs may have great therapeutic potential in patients with MS.
More importantly, current research together with data from migration studies opens the possibility that MS may be preventable in genetically susceptible individuals with early intervention strategies that provide adequate levels of hormonally active 1,25-dihydroxyvitamin D3 or its analogs.
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A growing body of evidence supports the hypothesis that vitamin D is an environmental factor important in the etiology of T-cell-mediated autoimmune diseases. Mechanistically, the 1,25(OH)2D3 targets in the immune system include CD4+T cells, DCs, and T reg (Table 1 and Fig. 1).
The net result of 1,25(OH)2D3 treatment in vivo is a reduction in the autoimmune Th1 response and an amelioration of symptoms of experimental IBD, RA, IDDM, and MS. Vitamin D receptor deficiency and vitamin D ligand deficiency both result in more severe experimental IBD.
Unexpectedly, IDDM and MS were less severe in VDR deficiency and more severe in vitamin D ligand deficiency. There may be both immune-mediated and target-organ-mediated effects of vitamin D in autoimmune diseases.
Clinical data confirming the connection between vitamin D and autoimmunity are lacking. New data in large prospective studies suggest that vitamin D supplementation reduces the incidence of RA, IDDM, and MS.
Patients with MS, IDDM, RA, or IBD express different VDR polymorphisms, which are associated with their disease, and have been shown to have low circulating levels of 25(OH)D3 and to be at an increased risk for bone fractures.
In areas with a high prevalence of autoimmunity, adequate vitamin D from the environment is difficult to acquire. Vitamin D supplementation is a safe and cost-effective way to increase circulating vitamin D levels.
More clinical trials using either vitamin D or 1,25(OH)2D3 analogs are needed. The risk of the 1,25(OH)2D3 analog treatments is hypercalcemia. However, new 1,25(OH)2D3 analogs may effectively regulate the immune system without increasing serum calcium.
Increasing circulating vitamin D is known to decrease the risk of bone fracture. An added benefit associated with increasing vitamin D intakes may be to decrease the incidence and severity of IDDM, MS, RA, and IBD. Improving vitamin D status in patients and relatives of patients with autoimmune disease should be a priority.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
Michelle M
Frequent Contributor (1K+ posts)
Member # 7200
posted
quote:Originally posted by klutzo: I must have a very bad case of Lyme brain this morning, becasue I read this three times and came up with the opposite conclusion.
It looks to me like this study concluded that the sun exposure made the Immune system less able to respond to the Bb, especially in terms of Lyme arthritis. I guess I can't understand research anymore, and it's very sad to keep losing brain function like this.
Klutzo
Klutzo, it's not just you, it's me, too.
Scientists are about as bad as lawyers in their inability to actually speak clearly.
Often you have to take the sentence apart, but when you do, you discover that you are exactly right.
"From these studies we concluded that UV irradiation can ... exacerbate the ... arthritic component of Lyme disease ..."
Now, so long as this doesn't result in taking anything out of context (and it doesn't appear to), it gets you to the bottom line:
SUNLIGHT MAKES ARTHRITIC LYME WORSE.
Michelle
Posts: 3193 | From Northern California | Registered: Apr 2005
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posted
Does this mean that the sun bed in the basement will make my arthritis pain worse? At least the little bit of tan makes me psychologically feel better.
Posts: 13 | From Fort Wayne, IN | Registered: Aug 2006
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kelmo
Frequent Contributor (1K+ posts)
Member # 8797
posted
On a paper the LLMD gave us, limiting sun exposure to 15 minutes daily, was one of the recommendations.
But, heat itself is good. If you can get in a 130 degree sauna for 30 minutes, it stimulates the metabolism and moves the bugs into the bloodstream.
When we are consistently going to the spa every day, my daughter feels better. We get complacent or sometimes the effort of getting in the car, and taking the following shower keeps us from going.
I don't have Lyme, and that first post with the research blew my mind. Is there someone who could put it into real words?
Posts: 2903 | From AZ | Registered: Feb 2006
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5dana8
Frequent Contributor (1K+ posts)
Member # 7935
posted
Thanks for posting the article david,very interesting.
we go to the carribian one week every year. while I am there I feel better than usual. Don't know if its the sun or soaking in the salt water or a combo of both.
But when I get back its more tired than usual. I think from the trip to get there?
I wish I could move there. Sigh
-------------------- 5dana8 Posts: 4432 | From some where over the rainbow | Registered: Sep 2005
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klutzo
Frequent Contributor (1K+ posts)
Member # 5701
posted
Michele, Thank you for making me feel a bit less brain dead. I feel much better when I get my 20 minutes of daily sun exposure, but I only have arthritis in my cervical and lumbar spine. My main problems are neurological.
Dana, I don't know where you live, but maybe we could trade places? I hate living in Florida. Just once I'd like to be able to take a simple walk around the block without having to peel off soaking wet clothes, and take a shower and wash my hair. I miss four seasons too. Yes, cold makes me hurt worse, but I still miss it.
Klutzo
Posts: 1269 | From Clearwater, Florida, USA | Registered: May 2004
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posted
I think they are saying when infected, sun exposure is not good.
My own experience would agree with this.
I used to be a regular sunbather, but now I am so sun sensitive that a brief exposure sends me into a flare.
Once I realized this was happening, I alos realized that all of my major intensifications happened in the summers. And that each summer I gradually got worse, losing a bit more function.
Though, of course, I did not come to see this pattern for years.
In fact until the last couple of years, I would have told anyone that asked that the sun made me better.
Posts: 845 | From Eastern USA | Registered: Jul 2006
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posted
I think I may have posted somewhere else about sun exposure but I will add my experiences here.
For the last few years I have become more and more sun-sensitive until now when I have to use total sun block when outdoors, even when driving a car when my hands are exposed through window glass.
Also, when in the sun very long (more than 30 minutes) I feel very drained.
I used to LOVE being in the sun and the beach (ocean waves, etc.) made me feel renewed. No longer.
I experience terrible rashes that itch like crazy. I have a pontoon boat docked at a local marina and I was only able to be on it 3 times this past summer. The drive to the marina plus the walk to the boat slip just does me in.
No doctor has yet been able to explain this sun-sensitivity. A recent visit to a dermatologist was downright humiliating...he gave me a sample of sunscreen with 30 block. I have to use TOTAL block. He was no help at all.
The derma doc did do tests for lupus and they all came back in normal range.
I have not yet been treated for Lyme. Am waiting on IgeneX tests to be sent to Dr. J in NC. Am also waiting on about 30 other tests he wanted done which I convinced my endocrinologist to order.
If my tests are not CDC positive I will be looking for another LLMD since Dr. J won't be able to help me.
I live in East TN and there are no LLMDs anywhere in my state that I can find. I project that I will be spending my life's savings in the coming year to 1 1/2 years just getting started with treatment.
I have Medicare HMO insurance and they will not pay for anything out of network.
This sun stuff is just an inconvience compared to all the other symptoms I have. I am trusting I will find the right doctor and the right treatment and will fight for this RIGHT!
Hope anything I said helps someone.
Janet
-------------------- DISCLAIMER: No information presented above should be considered medical advice or take the place of advice given by a medical professional. Links to other sites are provided merely for ease of research. Posts: 287 | From Tennessee | Registered: Sep 2006
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posted
The one thing that is missing, as far as whether we should follow the advice to get more vitamin D, is our current status of D in both 1,25 Dihydroxy and 25 Hydroxy vitamin D levels. I was loading up on vitamin D because of much of the research posted, and couldn't figure out why my 25 Hydroxy D levels remained low. Then I had my 1,25 Dihydroxy D levels check and they were high. They were beyond the high limit that is known to cause bone loss. No wonder I have Osteoporosis! What that means is that all that D I was supplementing was immediately converting to 1,25 Dihydroxy D and causing Osteo., not to mention other deleterious effects. (Like helping to proliferate Lyme.)
So, I suggest that anyone planning to supplement vitamin D should first have their 1,25 Dihydroxy levels checked first, because though you may test low in the usual 25 hydroxy test, you may be high in 1,25 dihydroxy, especially if you have Lyme Disease. Carol
Posts: 1 | From Spokane Valley | Registered: Oct 2006
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