IMMUUNIJÄRJESTELMÄ - A-VITAMIINI/BORRELIOOSI, AUTISMI

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Lähettäjä: Soijuv Lähetetty: 8.12.2004 12:36

Seuraavissa tutkimuksissa selvitellään mm. A-vitamiinin puutoksen yhteyttä autoimmuunitiloissa, esim. borrelioosin aiheuttamassa niveltulehduksessa:


Vitamin A deficiency is associated with a predisposition to Staphylococcus aureus infection in rats (4). The authors also reported that host defense mechanisms are profoundly affectedby Vitamin A deficiency.

Vitamin A deficiency is â??strongly associated with impaired immunity and infectious disease (5). Vitamin A deficiency impairs innate immunity and is also related to adaptive immunity (6).

Examples of autoimmune diseases associated with vitamin A deficiency include rheumatoid arthritis (7), juvenile arthritis (8 ), Lyme disease (9), systemic lupus (7), and insulin dependent diabetes mellitus (10, 11). Evidence has been reported from several studies that low vitamin A levels occurred in affected individuals before they became ill. In other words, the lack of vitamin A is associated with development of the disease and is not a consequence of them.

Med Hypotheses. 2000 Jun;54(6):979-83.

Is autism a G-alpha protein defect reversible with natural vitamin A?

Megson MN.

Pediatric and Adolescent Ability Center, Richmond, VA 23226, USA.

Autism may be a disorder linked to the disruption of the G-alpha protein, affecting retinoid receptors in the brain. A study of 60 autistic children suggests that autism may be caused by inserting a G-alpha protein defect, the pertussis toxin found in the DPT vaccine, into genetically at-risk children. This toxin separates the G-alpha protein from retinoid receptors. Those most at risk report a family history of at least one parent with a pre-existing G-alpha protein defect, including night blindness, pseudohypoparathyroidism or adenoma of the thyroid or pituitary gland.Natural vitamin A may reconnect the retinoid receptors critical for vision, sensory perception, language processing and attention. Autism spectrum disorders have increased from 1 in 10 000 in 1978 to 1 in 300 in some US communities in 1999. Recent evidence indicates that autism is a disorder of the nervous system and the immune system, affecting multiple metabolic pathways.

PMID: 10867750 [PubMed - indexed for MEDLINE]

This study of 60 autistic children and their families suggests that inserting a G-alpha protein defect, namely the pertussis toxin in the D.P.T. vaccine, (3) into genetically at-risk children causes autism. This toxin separates the G-alpha protein from retinoid receptors. Those most at risk report a family history of at least one parent with a pre-existing G-alpha protein defect, exhibited in disorders such as night blindness, pseudohypoparathyroidism or adenoma of the thyroid or pituitary gland (4).

This hypothesis asserts that treating these children with natural cis forms of Vitamin A may have the effect of reconnecting the hippocampal retinoid receptor pathways that are critical for vision, sensory perception, language processing and attention (5).

Many of these especially vulnerable children have tissue types of HREs DR 3, DR4, and DR5 (6). These particular tissue types form the tightest bonds with blocked RAR and RXR retinoid receptors (7).

Autism is a true developmental disorder. Many of these children are exposed to wheat at nine months, followed by exposure to the measles antigen at 12 to 15 months (8 ) The human measles antibody that is produced cross-reacts with intermediate filaments, which are known to be important for maintaining tight junctions and gap junctions between cells, gut mucosal integrity and cell to cell communication (10)(11).

Many of these children, who need natural, unsaturated cis forms of Vitamin A found in sources such as cold water fish like salmon, or cod, liver, kidney, and milkfat, are not getting this in the modern diet. Instead, they are dependent on Vitamin A Palmitate, found in commercial infant formula and lowfat milk. Unfortunately, absorption of Vitamin A Palmitate requires an intact gut mucosal microvilli surface at the right PH, in the presence of bile for metabolism (12). However, many of these children already have damaged mucosal surfaces due to unrecognized wheat allergy or intolerances.

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A monoclonal antibody to Borrelia burgdorferi flagellin modifies neuroblastoma cell neuritogenesis in vitro: a possible role for autoimmunity in the neuropathy of Lyme disease.

Sigal LH, Williams S.

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

Although Borrelia burgdorferi is found at the site of many manifestations of Lyme disease, local infection may not explain all features of the disease. Previous work has demonstrated that the organism's flagellin cross-reacts with a component of human peripheral nerve axon, heat shock protein 60. The cross-reacting epitope is identified by a single anti-B. burgdorferi flagellin monoclonal antibody, H9724. We now report that the spontaneous and peptide growth factor-stimulated in vitro neuritogenesis of SK-N-SH neuroblastoma cells and other neural tumor cell lines is suppressed by H9724. In contrast, changes induced by exposure of these cells to optimal and suboptimal concentrations of cyclic AMP, phorbol ester, or retinoic acid are not affected by H9724. H9724 does not decrease cell viability or the ability of the cells to anchor to the culture plate or extracellular matrix and does not block nerve growth factor binding to the cells. These findings are compatible with the premise that antiaxonal antibodies formed during the immune response to B. burgdorferi flagellin might modify axonal function in vivo and play a role in the pathogenesis of neurologic features of Lyme disease. A humoral immune response predicated on molecular mimicry could explain persistent or ongoing neurologic dysfunction occurring after elimination of the organism by appropriate antibiotic therapy.

PMID: 9125553 [PubMed - indexed for MEDLINE]
J Infect Dis. 1996 Oct;174(4):747-51. Related Articles, Links

Vitamin A deficiency exacerbates murine Lyme arthritis.

Cantorna MT, Hayes CE.

Department of Biochemistry, University of Wisconsin-Madison 53706, USA.

Vitamin A deficiency predisposes the host for a strong inflammatory response, suggesting that it may foster susceptibility to diseases, such as Lyme arthritis, in which activated macrophage and inflammatory cytokine production are pathogenic. Infected mice had a rapid serum retinal decline that correlated with the onset of arthritis. The mice with the least retinol developed acute arthritis earlier and more severely than those with the highest retinol. Earlier and stronger interleukin (IL)-12, interferon-gamma (IFN)-gamma, and tumor necrosis factor responses were found in Borrelia burgdorferi-infected, vitamin A-deficient mice compared with controls. The spirochetes induced IFN-gamma secretion from unprimed cells, and retinoid addition in vitro inhibited IFN-gamma synthesis. Vitamin A deficiency may exacerbate acute Lyme arthritis by enhancing an acute arthritogenic inflammatory response initiated by spirochete-driven IFN-gamma secretion. Conversely, vitamin A may lessen acute Lyme arthritis pathology by blocking IFN-gamma and IL-12 synthesis.

PMID: 8843212 [PubMed - indexed for MEDLINE]

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Fatty acids of Treponema pallidum and Borrelia burgdorferi lipoproteins.

Belisle JT, Brandt ME, Radolf JD, Norgard MV.

Department of Microbiology, University of Texas Southwestern Medical Center at Dallas 75235.

A fundamental ultrastructural feature shared by the spirochetal pathogens Treponema pallidum subsp. pallidum (T. pallidum) and Borrelia burgdorferi, the etiological agents of venereal syphilis and Lyme disease, respectively, is that their most abundant membrane proteins contain covalently attached fatty acids. In this study, we identified the fatty acids covalently bound to lipoproteins of B. burgdorferi and T. pallidum and examined potential acyl donors to these molecules. Palmitate was the predominant fatty acid of both B. burgdorferi and T. pallidum lipoproteins. T. pallidum lipoproteins also contained substantial amounts of stearate, a fatty acid not typically prevalent in prokaryotic lipoproteins. In both spirochetes, the fatty acids of cellular lipids differed from those of their respective lipoproteins. To characterize phospholipids in these organisms, spirochetes were metabolically labeled with [3H]palmitate or [3H]oleate; B. burgdorferi contained only phosphatidylglycerol and phosphatidylcholine, while T. pallidum contained phosphatidylglycerol, phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, phosphatidylinositol, and cardiolipin. Although palmitate predominated in the lipoproteins, there were no apparent differences in the incorporation of these two fatty acids into phospholipids (putative acyl donors). Phospholipase A1 and A2 digestion of phosphatidylcholine from B. burgdorferi and T. pallidum labeled with either [3H]palmitate or [3H]oleate also revealed that neither fatty acid was incorporated preferentially into the 1 and 2 positions (potential acyl donor sites) of the glycerol backbone. The combined findings suggest that fatty acid utilization during lipoprotein synthesis is determined largely by the fatty acid specificities of the lipoprotein acyl transferases. These findings also provide the basis for ongoing efforts to elucidate the relationship between lipoprotein acylation and the physiological functions and inflammatory activities of these molecules.

PMID: 8157583 [PubMed - indexed for MEDLINE]