Systemic lupus erythematosus (SLE)

Mayo Clinic overview

Amyloid-DNA Composites of Bacterial Biofilms A structured community of microorganisms encapsulated within a self-developed protective matrix and living together. Stimulate Autoimmunity. ¹⁾

We found that a component of bacterial biofilms, the amyloid protein curli, irreversibly formed fibers with bacterial DNA during biofilm A structured community of microorganisms encapsulated within a self-developed protective matrix and living together. formation. This interaction accelerated amyloid polymerization and created potent immunogenic complexes that activated immune cells, including dendritic cells, to produce cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. such as type I interferons, which are pathogenic in systemic lupus erythematosus (SLE).

Familial aggregationOccurrence of a given trait shared by members of a family (or community) that cannot be readily accounted for by chance. of lupus and autoimmunity in an unusual multiplex pedigree. ²⁾

OBJECTIVE: To evaluate an unusual pedigree with 8 members diagnosed with systemic lupus erythematosus (SLE)

METHODS: Pedigree members were evaluated through questionnaires, interviews, and medical records. Sixty members contributed serum samples for autoantibody analysis.

RESULTS: The 8 affected females shared several disease features, including arthritis (8/8), antinuclear antibodies (ANA) (8/8), pleuritis (6/8), malar rash (6/8), photosensitivityAbnormal sensitivity to sunlight and bright lights. Also referred to as "sun flare" or "light flare." (5/8), and nephritis (4/8). A total of 15 of 51 (29%) blood relatives had autoantibodies; 9 had autoimmune disease, including 7 with SLE, one with psoriasis, and one with Sjögren's syndrome. Five of 11 (45%) nonconsanguineous spouses also had autoantibodies; one spouse had SLE, and 2 others had thyroid disease. Among 68 spouses of patients with SLE in other pedigrees, only 9 (13%) had autoantibodies, and none were symptomatic (p = 0.02).

CONCLUSION: The high rate of autoimmunity among both blood relatives and nonconsanguineous mates in this unusual pedigree suggests a complex interaction of genetic and environmental factors contributing to disease.

Now, researchers at Temple University School of Medicine (TUSM) have shown that bacterial communities that form biofilms play a role in the development of the autoimmune disease systemic lupus erythematosus – a discovery that may provide important clues about several autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body ailments. ³⁾

Predictors of flare include rising anti-dsDNA antibody titres, proteinuria and CRP and B lymphocyte stimulator levels⁴⁾

Do classic blood biomarkers of JSLE identify active lupus nephritis? …Binary logistic regression modeling demonstrated a combination of ESR, C3, white cell count, neutrophils, lymphocytes and IgG to be best for the identification of active LN⁵⁾

Potential Immune Biomarkers in Diagnosis and Clinical Management for Systemic Lupus Erythematosus.⁶⁾

Monitoring disease activity in systemic lupus erythematosus with single-molecule array digital ELISA quantification of serum interferon-α.⁷⁾

Effects of 12-week Aerobic Exercise on Arterial Stiffness, InflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue., and Cardiorespiratory Fitness in Women with Systemic LUPUS Erythematosus: Non-Randomized Controlled Trial. ⁸⁾

Does minocycline have side effects or cause lupus?

https://pediatrics.aappublications.org/cgi/content/extract/101/5/926

The reports that Minocycline can induce lupus are laughable. Exactly how does a complex immune disease arise from the actions of a bacteriostatic antibiotic? Such a suggestion is ridiculous. The same goes for the suggestion that minocycline induces autoimmune hepatitis. Show us the beef, please - the molecular mechanisms.

In order to comprehend the discoveries springing from the cracking of the genome, today's physicians need to have a good understanding of modern science. It is tough for us to expect this, as many have not been even taught the basics of molecular biology. The alternative is for them to listen to those who are accepted as well grounded in science. Many physicians find that just as hard to swallow, as the profession trains them to present medicine, and its practitioners, to the public as infallible.

~Trevor

Once you understand the immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed. resulting from killing these Th1 pathogensThe community of bacterial pathogens which cause chronic inflammatory disease - one which almost certainly includes multiple species and bacterial forms., all these so-called side-effects are shown up for what they are - Immunopathology - and they disappear as you get rid of he pathogens.

..Trevor..

Mixed Connective Tissue Disease MCTD patients have rheumatic overlap syndrome plus anti-RNP antibodies. ^{9) 10)}

Antinuclear Antibody tests (ANA)

BACKGROUND: Excessive activity of dendritic cells (DCs) is postulated as a central disease mechanism in Systemic Lupus Erythematosus (SLE). Vitamin D is known to reduce responsiveness of healthy donor DCs to the stimulatory effects of Type I IFN. As vitamin D deficiency is reportedly common in SLE, we hypothesized that vitamin D might play a regulatory role in the IFNalpha amplification loop in SLE. Our goals were to investigate the relationship between vitamin D levels and disease activity in SLE patients and to investigate the effects of vitamin D on DC activation and expression of IFNalpha-regulated genes in vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory.. ¹¹⁾

Increased prevalence of vulnerable atherosclerotic plaques and low levels of natural IgM antibodies against phosphorylcholine in patients with systemic lupus erythematosus.

ABSTRACT: The risk of cardiovascular disease (CVD) and atherosclerosis is reported to be increased in systemic lupus erythematosus (SLE). We recently reported a negative association between natural IgM-antibodies against phosphorylcholine (anti-PC) in the general population, high anti-PC levels leading to decreased atherosclerosis development and low levels to increased risk of CVD. Potential mechanisms include anti-inflammatory properties and inhibition of uptake of oxidized low density lipoprotein (LDL) in macrophages. The objective herein was to study atherosclerosis in SLE in detail and in relation to traditional and non-traditional risk factors.

METHODS: 114 patients with SLE were compared with 122 age- and sex matched population-based controls. Common carotid intima-media thickness (IMT), calculated intima-media area (cIMa) and plaque occurrence were determined by B-mode ultrasound as a surrogate measure of atherosclerosis. Plaques were graded according to echogenicity and grouped as 1-4, with 1 being echoluscent, and considered most vulnerable. Anti-PC was studied by ELISA.

RESULTS: Hypertension, triglycerides and insulin resistance (determined by homeostasis model assessment of insulin resistance) and C-reactive protein (CRP) were increased in SLE (P < 0.01) while smoking, LDL, high density lipoprotein (HDL) did not differ between groups. Low levels of anti-PC IgM (lowest tertile) were more common in SLE patients than in controls (P = 0.0022). IMT and cIMa did not differ significantly between groups. However, plaques were more often found in SLE patients (P = 0.029). Age, LDL and IgM anti-PC (lowest tertile) were independently associated with plaque occurrence in SLE. Further, in the left carotid arteries echoluscent plaques (grade 1) were more prevalent in SLE as compared to controls (P < 0.016). CONCLUSIONS: Plaque occurrence in the carotid arteries is increased in SLE and is independently associated with age, LDL and low anti-PC levels. Vulnerable plaques were more common in SLE. Anti-PC could be a novel risk marker also with a therapeutic potential in SLE. ¹²⁾

Lupus Risk Linked To Staph Bacteria: Study

While the number of people diagnosed with lupus has more than tripled over the past four decades, researchers remain baffled, for the most part, as to what exactly causes the autoimmune disease.

In the study, published online this month in The Journal of Immunology, even small amounts of the pervasive bacteria (Staphylococcus aureus) caused mice to develop a lupus-like disease

The next step, Dr. Chowdhary explains, is to study lupus patients to see if the staph protein in question plays a similar role in humans. “Our hope is to confirm these findings in lupus patients and hopefully prevent flares,” he said in a release.

Lupus symptoms may come and go, but the times when a person is having symptoms are called flares, which can range from mild, such as dizzy spells or anemia, to severe, including pain or swelling in joints, red rashes and hair loss.

Mayo Clinic researchers are also hoping to uncover whether eradicating staph among people who are at risk for lupus can help prevent onset of the disease altogether.

Staph is commonly found on the skin or in the nose and can cause infections ranging from pneumonia to food poisoning. But skin infections are the most common, experts say, and are more likely to occur if you have a cut or scratch, or have contact with a person or surface that has staph bacteria. Dr Chowdhary's studies ^{13) 14) 15) 16) 17) 18)}

This Perspectives article discusses important questions about the use of ANA testing in both the clinical and research settings. ¹⁹⁾

This may indicate the importance of application of the test in a targeted way. ²⁰⁾

Ultraviolet (UV) light is an important environmental trigger for systemic lupus erythematosus (SLE) patients, yet the mechanisms by which UV light impacts disease are not fully known. This review covers evidence in both human and murine systems for the impacts of UV light on DNA damage, apoptosis, autoantigen exposure, cytokineAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. production, inflammatory cell recruitment, and systemic flare induction. In addition, the role of the circadian clock is discussed. Evidence is compared in healthy individuals and SLE patients as well as in wild-type and lupus-prone mice. Further research is needed into the effects of UV light on cutaneous and systemic immune responses to understand how to prevent UV-light mediated lupus flares.

UV exposure induces DNA damage, which can result in the formation of dimeric photoproducts involving neighboring pyrimidine bases (11–13). UV irradiation can also cause an accumulation of reactive oxygen species (ROS) in keratinocytes that results in oxidative damage to DNA, lipids, and proteins and can ultimately induce apoptosis (11, 13–15). Of importance, the oxidative damage to DNA bases can lead to formation of 8-hydroxyguanosine (8-OHG) which has been shown to be immunogenic in patients with lupus erythematosus (LE) and abundantly present in UV-induced LE lesions (16–18). ²¹⁾

When Chest Pain Reveals More: A Case of Hydrochlorothiazide-Induced Systemic Lupus Erythematosus. ²²⁾

Curli-Containing Enteric Biofilms Inside and Out: Matrix Composition, Immune Recognition, and Disease Implications. ²³⁾

Furthermore, curli (and extracellular DNA) of enteric biofilms potentiate the autoimmune disease systemic lupus erythematosus (SLE) and promote the fibrillization of the pathogenic amyloid α-synuclein, which is implicated in Parkinson's disease. Homologues of curli-encoding genes are found in four additional bacterial phyla, suggesting that the biomedical implications involved with enteric biofilms are applicable to numerous bacterial species.

Calcium and vitamin D supplement intake may increase arterial stiffness in systemic lupus erythematosus patients. ²⁴⁾

Patients receiving the highest dose of olmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. (40 and 80 mg) had an inward carotid remodeling and were shifted toward a lower elastic modulus at a given circumferential wall stress, indicating an improvement in the intrinsic elastic properties of the carotid artery wall material. These data suggest that 40 and 80 mg olmesartan were able to significantly remodel and destiffen the arterial wall material during long-term treatment, partly independently of blood pressure, compared with 20 mg. ²⁵⁾

Andreea Soare I was diagnozed with SLE.

I started MP 3 months ago. The first month was awful.

The second month, in the second part, things got incredibly better for about 3 weeks. I had my energy back Until 4rth of May when things stated to get worse everyday. All the symtomps seem to be back

Of course I have lost completly appetite and not only that but I feel repulsion towards almost all food.

My doctor recommanded me proton inhibitors 4 days ago. I took Nexium and then because there was no relief, he gave me Lanzap 30mg/day. I had to stop taking those proton inhibitors 2 days ago when I had an extremely painful period and also I vomitted .

The only thing which seems to have almost disappeared…at least for now, is my rash..

keithw “Hi Andreea, I also started with SLE and it is certainly a hard problem to fix but now I am 4 years into the protocol and I am symptom free.“

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