Nicotine can stop Cytokine Storm

Nicotine can stop Cytokine Storm


Ban Colloidal Silver. Try to ban vitamins and herbs. Try to ban organic gardening. Target smokers and ban smoking all over the country - then tax it so high that most can't afford to smoke !!

NOW READ THIS !!

http://coloyan.com/blog/2009/04/28/swine-flu-smoke-em-if-you-got-it/


Swine Flu? Smoke em if you got it; Nicotine can stop Cytokine Storm

By Administrator

What often kills people who catch Swine Flu is not the virus itself but the body’s immune system reaction which is called a cytokine storm. Ironically this often occurs in young, healthy people with good immune systems which is why the Swine Flu seems to be more dangerous to people between 20-50.

“If a cytokine storm occurs in the lungs, for example, fluids and immune cells such as macrophages may accumulate and eventually block off the airways, potentially resulting in death”

While this may sound completely insane, there have been studies showing that nicotine can reduce a cytokine storm and the ensuing inflammation. One such article detailing this information was “Body Blazes” by Lisa Melton published in Scientific American in June 2006. For a full text of the article :

Body Blazes
Lisa Melton
Scientific American; Jun2006, Vol. 294 Issue 6, p24-24, 1p, 1 color

HOW NICOTINE STOPS INFLAMMATION COULD LEAD TO NEW DRUGS

* Nicotine has undergone * an image overhaul, at least biomedically. In the past few years researchers have found that the substance can alleviate symptoms of ailments such as Alzheimer's disease and ulcerative colitis. Just how nicotine battles these foes, however, has remained unclear. Now, by studying sepsis, Luis Ulloa of North Shore University Hospital in Manhasset, N.Y., has evidence elucidating
nicotine's biochemical pathways that could lead to more potent anti-inflammatory drugs.

Sepsis, the most lethal of inflammatory conditions, is a bacterial invasion of the bloodstream. The third leading cause of death in the developed world, it accounts for nearly 10 percent of overall deaths in
the U.S. every year. Infection causes part of the damage, but what makes patients critically ill is their own fiercely aggressive immune response. Macrophages churn out huge quantities of proinflammatory cytokines. This exaggerated immune response leads to tissue damage, and eventually the patient dies of cardiovascular dysfunction and multiorgan failure.

Ulloa and his collaborators have found something remarkable: nicotine can shut down this overshooting inflammatory response, to the point of reversing sepsis in mice. As far as anti-inflammatory treatments go, this is powerful stuff. "Nicotine taps into the body's own potent anti-inflammatory mechanisms," Ulloa explained in February at a Novartis
Foundation meeting in London. "That is the beauty of our approach. By using nicotine, we are copying physiological mechanisms that have been selected by evolution to modulate the immune system."

Specifically, nicotine mimics acetylcholine, the Cinderella of neurotransmitters. Largely ignored over the years, acetylcholine has been catapulted into a starring role, linking the nervous and the immune
systems. Through acetylcholine the nervous system controls the inflammatory fires that constantly crop up in our bodies. Receptors for acetylcholine reside not only on nerve cell endings but also on immune
cells. Nicotine binds and activates these receptors, allowing cross talk between the brain and immune system.

"This is something quite phenomenal," comments Wouter de Jonge of the Academic Medical Center Amsterdam, who studies how macrophages respond to acetylcholine. "Smokers suffering from ulcerative colitis seemed to benefit from their habit, so there were hints that nicotine could ameliorate inflammatory diseases, but nobody could get a handle on it," he notes.

Now Ulloa's group may have provided an explanation for the positive effects that nicotine has on illnesses as diverse as schizophrenia,
Alzheimer's, Parkinson's disease, Tourette's syndrome and ulcerative colitis. In laboratory experiments, Ulloa demonstrated that nicotine latches onto the nicotinic receptors on macrophages and stops them from
spewing out inflammatory cytokines. This clampdown is brutally effective. The researchers also identified the specific receptor subtype, the alpha-7 acetylcholine receptor, that nicotine binds in
macrophages to stop cytokine production.

But as a drug, nicotine is fraught with toxicity issues. Apart from its addictive nature, it can lead to cardiovascular problems and contribute to cancer. "No one is looking to use nicotine to treat inflammation," Ulloa says. "We want to design specific compounds that will target this
receptor to take advantage of nicotine's anti-inflammatory effects while eluding its collateral toxicity."

"This is one of the great stories in immunology in the past few years—no question about it," remarks Mitchell Fink, an expert in critical care
medicine at the University of Pittsburgh. A selective nicotinelike compound may be a promising therapy not only for sepsis but for a whole slew of chronic conditions, including heart disease, cancer and
diabetes. The task at hand is to find the best surrogate for nicotine.

Ulloa's petri dishes are the ones to watch.

A NICK OF NICOTINE

As a potent anti-inflammatory, nicotine can damp down a dangerous immune response. But it is too risky as a treatment. Fortunately, substitutes may exist. Pharmaceutical firms have developed nicotinelike drugs, such as GTS-21, that were designed to stimulate the alpha-7 acetylcholine receptors in the brains of patients with Alzheimer's disease. But the
clinical trials failed to show a clear benefit, and the drugs were dropped. The compounds may have been unable to cross the blood-brain barrier—which would actually be a plus for an anti-inflammatory, because
then it could target the periphery and avoid the brain. Researchers have begun testing such substitutes to combat inflammation.