Inflammation connections - includes cells, bugs and genes that might connect one disease to another. To what extent does one inflammation disease increase your risk for another - and why?

Looking at the connections might help reveal what's really going on.

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ALL INFLAMMATION CONNECTIONS POSTS

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December 15, 2009

Role of estrogen in trigeminal nerve sensitization

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Estrogen plus inflammation acts via trigeminal nerve to increase pain in TMJ and perhaps migraine.

The highest incidence of TMJ is observed in women between 20 and 40.

The authors note that TMJ is associated with estrogen. Their investigation concerned the possible mechanism by which estrogen might act as a risk factor in the development of TMJ.

They found that inflammation plus estrogen increased pain perception via the trigeminal nerve through a MAPK pathway.

The MAPK pathway does interact with NF-kB, but the primary point of interest here is the overlap with migraine. Migraine is also predominant in women (approximately two to three times as many women suffer with migraine as men.) Migraine is also most prevalent between ages 20 and 40. The trigeminal nerve is also central in migraine pain.

It may be that migraine and TMJ share, at least to some extent, the same underlying pathology.

Estrogen is generally anti-inflammatory and is considered ‘protective’ against certain conditions associated with inflammation (e.g. atherosclerosis.)  Nonetheless, many of the conditions most closely associated with inflammation (e.g. autoimmune conditions) are far more common in women.

If the reason for this apparent paradox could be determined, it might be of great assistance in developing effective treatments for conditions associated with inflammation.

The publication:

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Neuroscience. 2009 Dec 29;164(4):1813-20. Epub 2009 Sep 25.

Chronic inflammation and estradiol interact through MAPK activation to affect TMJ nociceptive processing by trigeminal caudalis neurons.

Tashiro A, Okamoto K, Bereiter DA.

Department of Diagnostic and Biological Sciences, University of Minnesota School of Dentistry, 18214 Moos Tower, Minneapolis, 515 Delaware Street SE, Minneapolis, MN 55455, USA.

Summary of the abstract

The mitogen-activated protein kinase/extracellular regulated kinase (MAPK/ERK) pathway plays a key role in mediating estrogen actions in the brain and neuronal sensitization during inflammation.

Estrogen status is a risk factor in chronic temporomandibular muscle/joint (TMJ) disorders; however, the basis for this relationship is not known. The present study tested the hypothesis that estrogen status acts through the MAPK/ERK signaling pathway to alter TMJ nociceptive processing.

These results suggested that estrogen status and chronic inflammation acted, at least in part, through a common MAPK/ERK-dependent signaling pathway to enhance TMJ nociceptive processing by laminae I-II neurons at the spinomedullary junction region.

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December 6, 2009

Neurotransmitters and inflammation

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Acetylcholine, a neurotransmitter, exerts an anti-inflammatory effect, probably by inhibiting NF-kB.

This may, at least in part, explain certain neurotransmitter imbalances and other central nervous system abnormalities associated with inflammatory conditions.

The publication:

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Med Sci Monit. 2007 Dec;13(12):RA214-21.

Acetylcholinesterase and butyrylcholinesterase as possible markers of low-grade systemic inflammation.

Das UN.

UND Life Sciences, Shaker Heights, OH 44120, USA.

Summary of the abstract

Insulin resistance, obesity, type 2 diabetes, high blood pressure, hyperlipidemias, metabolic syndrome X, and Alzheimer’s disease are characterized by low-grade systemic inflammation.

Recent studies showed that the plasma and tissue activities of two enzymes, butyrylcholinesterase and acetylcholinesterase,  are both elevated in patients with Alzheimer’s, diabetes, high blood pressure, insulin resistance, and hyperlipidemia. High levels of these two enzymes result in low plasma and tissue levels of acetylcholine (ACh).

The “cholinergic anti-inflammatory pathway” mediated by acetylcholine acts by inhibiting the production of pro-inflammatory mediators, probably by inhibiting NF-kB.

ACh is a neurotransmitter and regulates the levels and activities of serotonin, dopamine and other neuropeptides and thus, modulates both immune response and neurotransmission.

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November 21, 2009

Alzheimer’s & arthritis – inflammation can’t turn off

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Deficient NF-kB inhibitor (CARD8) in Alzheimer’s and rheumatoid arthritis

The two studies briefly summarized below are consistent with the theory that excess inflammation often results from the body’s inability to shut down NF-kB – the Master Switch of inflammation.

Turning on NF-kB results in inflammation. If NF-kB cannot be turned off, chronic inflammation results.

One of many ways the body turns off NF-kB is with a protein messenger known as “CARD8.” Normally, CARD8 is made when NF-kB is activated. The negative feedback loop (the result of turning on NF-kB is a product that feeds back and turns off NF-kB) is one reason inflammation does not normally get out of hand.

A genetic defect has been identified that results in less effective CARD8. Less effective CARD8 means the normal, negative feedback loop that helps keep inflammation in check is missing – so inflammation continues.

This defect in CARD8 has been identified as a contributor to Alzheimer’s and rheumatoid arthritis. Some studies have suggested that defective CARD8 might also be associated with Crohn’s disease.

What seems clear is that CARD8 is only one of many ways the body keeps inflammation in control. To the extent that this and other defects result in deficient NF-kB inhibitors, supplementing NF-kB inhibitors, as suggested on this site, might be helpful.

In the first study below, defective CARD8 was found to increase the risk of developing Alzheimer’s 2.4x in women.

In the second study below, defective CARD8 was found to predict the severity of rheumatoid arthritis.

The first publication:

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Dement Geriatr Cogn Disord. 2008;26(3):247-50. Epub 2008 Oct 8.

Deficiency of CARD8 is associated with increased Alzheimer’s disease risk in women.

Fontalba A, Gutiérrez O, Llorca J, Mateo I, Berciano J, Fernández-Luna JL, Combarros O.

Unidad de Genética Molecular, Marqués de Valdecilla University Hospital, Santander, Spain.

Summary of the abstract

NF-kB, a major transcription factor controlling inflammation, is activated in Alzheimer’s disease (AD) brains.

CARD8 protein has been implicated in the suppression of NF-kB activity, but a slight genetic alteration makes CARD8  non-functional and results in more active NF-kB and an amplification of the inflammatory process.

The major genetic risk factor of AD, is associated with hyperactivation of NF-kB and enhanced brain inflammation.

In a case-control study in 300 AD patients and 300 healthy controls, we examined whether the slight genetic alteration leading to non-functional CARD8 might predispose to AD. Women, but not men, had a 2.39-fold higher risk of developing AD than subjects without the alteration.

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The second publication:

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J Immunol. 2007 Oct 1;179(7):4867-73.

Deficiency of the NF-kappaB inhibitor caspase activating and recruitment domain 8 in patients with rheumatoid arthritis is associated with disease severity.

Fontalba A, Martinez-Taboada V, Gutierrez O, Pipaon C, Benito N, Balsa A, Blanco R, Fernandez-Luna JL.

Unidad de Genetica Molecular, Hospital Universitario Marques de Valdecilla, Santander, Spain.

Summary of the abstract

CARD8 potently inhibits NF-kappaB signaling, which plays a key role in inflammation, and may contribute to avoid a pathologic activation of NF-kB; however, the transcriptional mechanisms regulating CARD8 expression and the relevance of this protein in inflammatory diseases are poorly understood.

To study the relevance of CARD8 in chronic inflammatory disorders, we functionally characterized a deleterious polymorphism (p.C10X) and studied its association with rheumatoid arthritis (RA).

Deficiency of CARD8 was found to predict the severity of rheumatoid arthritis.

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November 21, 2009

Diabetes links to Alzheimer’s

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Type 2 diabetes has been found to increase the risk of developing Alzheimer’s disease.

Both Alzheimer’s and type 2 diabetes are associated with excess inflammation. NF-kB may be the critical link between these two conditions.

The publication:

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J Alzheimers Dis. 2009 Apr;16(4):809-21.

Inflammation and NF-kappaB in Alzheimer’s disease and diabetes.

Granic I, Dolga AM, Nijholt IM, van Dijk G, Eisel UL.

Department of Molecular Neurobiology, University of Groningen, Haren, The Netherlands.

Summary of the abstract

Inflammatory processes are a hallmark of many chronic diseases including Alzheimer’s disease and diabetes mellitus.

Fairly recent statistical evidence indicating that type 2 diabetes increases the risk of developing Alzheimer’s disease has led to investigations of the potential common processes that could explain this relation.

This publication reviews how NF-kB might be involved in both diabetes mellitus and Alzheimer’s disease.

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November 21, 2009

Simvastatin (Zocor) inhibits NF-kB, reduces inflammation

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Zocor inhibits NF-kB and so might be useful in the treatment of many conditions related to inflammation.

Inhibition of NF-kB will produce beneficial effects in conditions related to inflammation.

Of interest, NF-kB inhibition has a direct, and favorable, impact on lipids. Perhaps NF-kB inhibition is more than just a beneficial ’side effect’ of statins. Perhaps some of the cholesterol lowering effect of statins results from their ability to inhibit NF-kB.

Expect to see more effort directed toward promoting the use of statins in the treatment or prevention of conditions related to inflammation. For example, here is a discussion of the possible use of statins in preventing cancer.

But keep in mind that statins may be relatively weak inhibitors of NF-kB, that they can have undesirable side effects. We already have a wide assortment of NF-kB inhibitors available for use. Your kitchen is (I hope) full of them – essentially every fruit or vegetable is an NF-kB inhibitor.

If you want something a little more effective than your ‘garden variety’ fruit or vegetable, select from curcumin (the active ingredient in turmeric) or one of the many other herbs that has a long history of medicinal use and that has been shown to inhibit NF-kB.Relative to the statins, these alternatives are less expensive, safer, and almost certainly more effective inhibitors of NF-kB.

The publication:

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Shock. 2009 Aug;32(2):159-63.

Simvastatin reduces endotoxin-induced nuclear factor kappaB activation and mortality in guinea pigs despite lowering circulating low-density lipoprotein cholesterol.

Fraunberger P, Gröne E, Gröne HJ, Walli AK.

Medical Central Laboratories, Feldkirch, Austria.

Summary of the abstract

Statins, which are effective lipid-lowering drugs, also possess anti-inflammatory potential.

The same lipids that are reduced by treatment with simvistatin might be helpful in fighting inflammation, especially as they counter the effects of bacterial toxins. It is thus paradoxical that statins, which drastically reduce circulating cholesterol levels, should be beneficial in patients with inflammatory disease.

The effect of simvastatin on NF-kB was investigated, and simvistatin was found to be associated with a significant reduction in NF-kB activation.

The data suggest that simvastatin, despite lowering circulating low-density lipoprotein cholesterol, had an anti-inflammatory effect by means of its inhibition of NF-kB.

Simvistatin therefore deserves consideration as a possible supplementary therapy in acute inflammatory disease.

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November 19, 2009

Profound improvement in psoriasis

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Topical or systemic application of extract results in profound improvement in mouse model of psoriasis

This publication is really quite remarkable.

First, it’s seldom that researchers will use a phrase like “profound improvement.” Researchers tend toward understatement, not hyperbole. The mouse must truly have been ‘cured’ to elicit such a statement.

Second, the extract was equally effective whether applied topically, or administered systemically.

Finally, this effect was achieved with an extract that has been in use for thousands of years.

What is acetyl-11-keto-beta-boswellic acid (AKbetaBA)? It’s a a naturally occurring gum resin isolated from the  stem of the tree Boswellia serrata. It’s frankincense. Yes, just like in the Nativity story.

Impressive results – natural product. If I had psoriasis (and didn’t have Banjo) I would be out looking for frankincense.

But is it safe? Well, for starters it’s edible (when pure.) That’s always a good sign. Plus it has a 5,000 year history of safe use – and an equally long history of medicinal use. In Ayurvedic medicine frankincense is recommended for the treatment of arthritis. In Asia it has been used for digestive problems and as a treatment for skin conditions. I would do some additional research before using it myself – and a lot more research before giving it to anyone else – but based on what I already know, it’s likely safe. And likely much safer than most other treatments.

And since it’s an NF-kB inhibitor it will do more than just treat the symptoms of psoriasis. It would likely lesson the chance of psoriatic arthritis while inhibiting colon cancer, (and prostate cancer, and multiple myeloma) lowering your cholesterol, treating your osteoarthritis, and reducing symptoms in chronic colitis, ulcerative colitis, Crohn’s disease, bronchial asthma and a host of other ailments too long to list.

That’s what natural NF-kB inhibitors do. Some do it (much) better than others. But they all do it – because they fight inflammation.

And you’re already using them. Every fresh fruit and vegetable is a natural NF-kB inhibitor.

But you’re probably not using enough of them, especially because our modern world is filled with so many things that cause inflammation. And if you have an autoimmune disease – like psoriasis – then you have a genetic vulnerability to inflammation. You need even more of these NF-kB inhibitors.

With additional NF-kB inhibitors from frankincense (or Banjo) – you can get better. That’s my theory. It’s not proven, but it’s consistent with the results from thousands of studies, a few of which are referenced on this site – one of which is summarized below.

The publication:

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J Immunol. 2009 Oct 1;183(7):4755-63. Epub 2009 Sep 14.

Targeting NF-kappa B with a natural triterpenoid alleviates skin inflammation in a mouse model of psoriasis.

Wang H, Syrovets T, Kess D, Büchele B, Hainzl H, Lunov O, Weiss JM, Scharffetter-Kochanek K, Simmet T.

Summary of the abstract

Psoriasis vulgaris is a common chronic inflammatory skin disease involving cytokines and an activated cellular immune system.

At variance to skin from patients with atopic dermatitis or from healthy subjects, human psoriatic skin lesions exhibit strong activation of transcription factor NF-kappaB.

Since NF-kappaB signaling is required for the induction of many cytokines, and since aberrant cytokine expression has been proposed as the cause of psoriasis, we investigated – using a mouse model – whether NF-kappaB targeting would affect the course of the disease.

When mice with severe psoriatic lesions were treated systemically or locally with the IkappaB kinase inhibitor acetyl-11-keto-beta-boswellic acid (AKbetaBA), NF-kappaB signaling and cytokine production were profoundly suppressed.

Additionally, application of the compound counteracted the expression of pro-inflammatory cytokines in previously diseased skin areas. Inflammation resolved and skin cell hyper-proliferation ceased.

Overall, the treatment was accompanied by a profound improvement of the psoriasis.

Our data demonstrate that NF-kappaB signaling is pivotal for the pathogenesis of psoriasis in the mouse model. Therefore, targeting NF-kappaB might provide an effective strategy for the treatment of psoriasis.

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November 18, 2009

NF-kB: Autoimmunity Master Switch

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A review of NF-kB and autoimmune disease

The abstract below is a quick overview. It suggests the central importance of NF-kB and then lists a few of the autoimmune conditions related to excess NF-kB activation.

The full text article provides a more thorough review, and is available free online.

The full article includes a number of challenges and potential dangers associated with pharmaceutical inhibition of NF-kB. Please note, however, that on this site I’m mainly discussing NF-kB inhibition by means of natural extracts. You’re already doing that – every day – it’s just that you might not be doing enough of it, especially since we’re all exposed to more inflammation promoters every day.

Of course natural extracts are not necessarily safe. Some can have side effects at high doses, and some are outright poisonous.

So as an added safety precaution, Banjo uses only those ingredients that have at least a 1,000 year history of safe use and for which no dose, however great, has ever been found unsafe. Then Banjo uses a relatively small amount of each extract, but in combination with a unique “trans-mucosal” delivery system, it’s very effective.

So yes – NF-kB inhibition by synthetic pharmaceuticals will probably cause all sorts of side effects.

But the natural extracts? If it was possible to overdose I’d be long gone. I drink a lot of coffee.

The publication:

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Acta Biochim Pol. 2008;55(4):629-47. Epub 2008 Dec 16.

The role of nuclear factor-kappaB in the development of autoimmune diseases: a link between genes and environment.

Kuryłowicz A, Nauman J.

Summary of the abstract (or you can read the free full text online)

Although autoimmune diseases are relatively common, mechanisms that lead to their development remain largely unknown.

Nuclear factor-kappaB (NF-kappaB), as a key transcription factor involved in the regulation of immune responses and apoptosis, appears to be a good candidate for studies on the pathogenesis of autoimmunity.

This review presents how perturbations of the NF-kappaB signaling pathway may contribute to self-tolerance failure, initiation of autoimmune inflammatory response as well as its persistent maintenance and therefore to the development of common autoimmune diseases including:

  • rheumatoid arthritis
  • multiple sclerosis
  • diabetes
  • thyroid autoimmune diseases
  • lupus
  • inflammatory bowel diseases
  • and psoriasis

A special emphasis is put on the genetic variations in the NF-kappaB related genes and their possible association with susceptibility to autoimmune diseases, as well as on the therapeutic potential of the NF-kappaB targeted strategies in the treatment of autoimmunity.

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November 18, 2009

Colorectal cancer and inflammatory bowel disease

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Colorectal cancer more common with inflammatory bowel disease, especially ulcerative colitis

Over-activation of NF-kB is now recognized as a major contributor to inflammatory bowel disease and cancer. NF-kB activation results in inflammation, obviously of significance in inflammatory bowel disease, but increasingly recognized as central to carcinogenesis.

The relative cancer risk increases with the duration and severity of inflammatory bowel disease.

The publication:

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Curr Drug Targets. 2008 May;9(5):375-80.

Cytokines: from gut inflammation to colorectal cancer.

Fantini MC, Pallone F.

Summary of the abstract

Colorectal cancer represents a life-threatening complication of inflammatory bowel diseases.

Statistics indicate that the risk to develop colorectal cancer is higher in patients affected by ulcerative colitis and to a lesser extent by Crohn’s disease and that such a risk is directly proportional to the number of years of active disease.

These observations suggest that chronic inflammation may substantially contribute to cancer development.

However the molecular mechanisms underlying this process have been only recently started to be clarified. It is now becoming clear that the large amount of cytokines and growth factors released during inflammation by immune and non immune cells may influence the carcinogenesis process.

IL-6 and IL-23, cytokines which play key roles in the induction and maintenance of gut inflammation during IBDs, have been recently shown to influence the development and growth of colitis associated colorectal cancer.

Moreover, the activation of the nuclear factor kappa B (NF kappa B), a transcription factor activated by several cytokines released during inflammation and responsible for many of their proinflammatory effects, have been shown to promote the growth of the colon tumors in experimental models.

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November 18, 2009

Probiotics for Crohn’s disease and ulcerative colitis

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Lactobacillus inhibits NF-kB

The term “probiotic” is used to describe organisms that are used medicinally, including bacteria such as Lactobacillus.

Lactobacillus bacteria are normally found in the small intestine. These are ‘good bacteria’ since they produce vitamin K as well as certain anti-microbial substances which prevent the ‘overgrowth’ of harmful bacteria.

A number of human trials have reported benefits associated with lactobacillus administration for the inflammatory bowel conditions ulcerative colitis and Crohn’s disease.

Lactobacillus has also been shown to benefit asthma patients.

While lactobacillus is generally helpful, the specific means by which it benefits patients with inflammatory bowel disease was uncertain. Researchers have now determined that lactobacillus exerts it anti-colitis effect through inhibition of NF-kB.

The publication:

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Int J Colorectal Dis. 2009 Feb;24(2):231-7. Epub 2008 Dec 3.

Lactobacillus suntoryeus inhibits pro-inflammatory cytokine expression and TLR-4-linked NF-kappaB activation in experimental colitis.

Lee JH, Lee B, Lee HS, Bae EA, Lee H, Ahn YT, Lim KS, Huh CS, Kim DH.

Summary of the abstract

OBJECTIVE: Lactic acid bacteria (LAB) can improve disturbances of indigenous microflora as well as inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn’s disease.

We examined the anticolitic effect of Lactobacillus, which is known to inhibit NF-kappaB activation, in a mouse model of colitis.

RESULTS AND DISCUSSION: In the mouse model of colitis we saw colon shortening and also increased markers of inflammation. However, oral administration of Lactobacillus inhibited colon shortening and decreased the level of inflammation markers. Lactobacillus inhibited the NF-kappaB activation, as well as the expression of COX-2.

CONCLUSION: Lactobacillus can improve colitis via the inhibition of NF-kappaB activation.

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November 18, 2009

NF-kB receptor problem common to rheumatoid arthritis, psoriasis & Crohn’s Disease

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One common effect of NF-kB over-activation in Rheumatoid arthritis, psoriasis & Crohn’s Disease

Key points:

  • A receptor [A(3)AR] is associated with inflammation.
  • It turns out that in rheumatoid arthritis, psoriasis and Crohn’s, there is ‘too much’ of this receptor on peripheral blood mononuclear cells (PBMCs) – a common thread.
  • These same PBMCs also have ‘too much’ activated NF-kB – the ultimate common thread.

The publication:

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Cell Immunol. 2009;258(2):115-22. Epub 2009 May 7.

The anti-inflammatory target A(3) adenosine receptor is over-expressed in rheumatoid arthritis, psoriasis and Crohn’s disease.

Ochaion A, Bar-Yehuda S, Cohen S, Barer F, Patoka R, Amital H, Reitblat T, Reitblat A, Ophir J, Konfino I, Chowers Y, Ben-Horin S, Fishman P

Summary of the abstract

The Gi protein associated A(3) adenosine receptor (A(3)AR) was recently defined as a novel anti-inflammatory target.

The aim of this study was to look at A(3)AR expression levels in peripheral blood mononuclear cells (PBMCs) of patients with autoimmune inflammatory diseases and to explore transcription factors involved receptor expression.

Over-expression of A(3)AR was found in PBMCs derived from patients with rheumatoid arthritis (RA), psoriasis and Crohn’s disease compared with PBMCs from healthy subjects.

Bioinformatics analysis demonstrated the presence of DNA binding sites for nuclear factor-kappaB (NF-kappaB) and cyclic AMP-responsive element binding protein (CREB) in the A(3)AR gene promoter.

Up-regulation of NF-kappaB and CREB was found in the PBMCs from patients with RA, psoriasis and Crohn’s disease.

NF-kappaB and CREB are involved with the over-expression of A(3)AR in patients with autoimmune inflammatory diseases.

The receptor may be considered as a specific target to combat inflammation.

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November 18, 2009

Lupus, Asthma & NF-kB

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Dendritic cells stimulate the immune system by presenting antigens (foreign particles) to other immune cells and by causing the release of pro-inflammatory cytokines. It is believed that dendritic cells may play an important role in autoimmune disease.

The serum from patients with lupus causes monocytes to transform into dendritic cells and is associated with increased NF-kB activation.

The serum from patients with asthma also causes monocytes to transform into dendritic cells and is associated with increased NF-kB activation.

Inhibition of NF-kB contributes to T cell tolerance – by which is meant tolerance to self. When “tolerant” T cells do not attack self. T cell intolerance may lead to autoimmune disease.

Read the full article »

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November 18, 2009

Migraine associated with multiple sclerosis

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Headache is not generally considered as a symptom of multiple sclerosis (MS), but several studies have showed that it is more frequent (about 50%) in MS patients than in controls or general population.

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November 16, 2009

Rheumatic impact of IBD

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Common musculoskeletal conditions among those with inflammatory bowel disease – arthritis and fibromyalgia.

Three observations suggest that we might be looking at a single underlying mechanism of disease.

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November 16, 2009

Enbrel inhibits NF-kB

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Etanercept (Enbrel) inhibits NF-kB when used in the treatment of psoriatic arthritis. The immune system is extremely complex and includes many feedback loops (positive and negative) as well as much ‘cross talk’ between its various components. The relationship between NF-kB and TNF is defined (in part) by a positive feedback loop.

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November 10, 2009

Better by Christmas – with Frankincense

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At first it’s hard to believe that any one thing could effectively treat so many ailments. But since NF-kB inhibitors fight inflammation, it makes sense. If inflammation contributes to the cause of many conditions (and it does) then whatever relieves inflammation (actually treating the cause, not just masking the symptoms) should be effective in treating many ailments.

Read the full article »

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November 6, 2009

NF-kB: Crohn’s, RA, lupus, psoriasis

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NF-kB is the master regulator – the primary means by which inflammation is ‘adjusted’ – turned on and off. Many, many different molecules interact with NF-kB – some stimulating it (increasing inflammation) and others inhibiting it (decreasing inflammation.) The balance between these positive and negative forces determines the extent of inflammation at any given time.

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September 1, 2009

Novel genetic finding: Crohn’s

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Researchers have discovered a link between a gene that regulates inflammation and the gene most frequently associated with Crohn’s disease.
[stextbox id="grey"]Derek Abbott, M.D., Ph.D., and his team of researchers found that ITCH also influences NOD2-induced inflammation. These findings, published in the August 11th issue of Current Biology, suggest a common pathophysiology exists [...]

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