Inflammation characterized by multiple chronic

The immune system is a complex array of organs, tissues and specialized cells that protect us from foreign invaders such as bacteria, viruses, allergens and harmful to insiders, such as infected cells and toxins. Sometimes the immune system turns on itself, hence the name >> << tissue damage and produces substances that generate chronic diseases. Examples include autoimmune disease in diabetes mellitus type 1 (insulin dependent), multiple sclerosis, rheumatoid arthritis and systemic lupus erythematosus. Treatment of body

-(PUFAs) participate in any of these conditions. A protective effect on the immune system response that combats bacteria and other infectious agents. But when >> << are excessive because they are in asthma and rheumatoid arthritis, they result in redness, swelling, pain, stiffness and other symptoms. Inflammatory responses due to wheezing and difficulty breathing in asthma, inflammation of the kidneys in nephritis, itching eczema, and red blisters from insect bites and allergic dermatitis. Many drugs work to stop excessive inflammation. Inflammation characterized by multiple chronic diseases such as atherosclerosis (clogged arteries). Inflammation develops in tissues such as blood vessels, lung, connective tissue and partly due to activities that protect cells from clearing unwanted particles invading organisms and toxins (Fig. 1). However, the enemy side activity of macrophages is the production of proinflammatory substances that worsen atherosclerosis. Including induced food and inhaled particles such as pollen and dust mites. Sensitive or allergy sufferers react to harmless substances >> << start the immune response. For example, some products mites, pollen and dust can cause allergic reactions. In allergies, the immune system produces a large number of antibodies, especially called IgE. Interaction of allergen with IgE causes a cascade of events resulting in allergic symptoms (Fig. 2). Polyunsaturated fatty acids in inflammation are precursors of substances that can promote or limit inflammation. As a group, these substances are called. The most common eicosanoids are from, omega-6 PUFAs. These eicosanoids promote blood clotting that can lead to heart attack and stroke and help

education in the walls of blood vessels. They also generate

mediators of inflammation, which damage blood vessel walls. In the lungs and airways, another type of arachidonic acid derived eicosanoids,, narrow respiratory muscles makes breathing more difficult lasix 40 meq. Leukotrienes can cause asthma attacks. Antiasthmatic drugs interact with leukotriene activity. PUFAs found in fish oil, mainly

(docosahexaenoic acid) suppress and counter-action of arachidonic acid derived eicosanoids. For environmental protection, in particular, competes with arachidonic acid for inclusion in the cell membrane. Through this competition, it reduces the amount of arachidonic acid for the production of eicosanoids. In addition, the environment creates a type of eicosanoids that are less powerful inflammatory >> << activities than those of arachidonic acid. Working to stop the inflammatory activity. This means that arachidonic acid is actively involved in promoting and ends inflammatory response. Similarly, EPA also creates a substance called "resolvins", which will accelerate the end of inflammation. Aspirin facilitates the production and lipoxins resolvins. Thus, fish oil PUFAs against inflammatory activity by reducing the production of inflammatory mediators, producing weaker eicosanoids and increased production of substances that stop inflammation. As a result, they reduce the inflammatory symptoms of asthma, rheumatoid arthritis, atherosclerosis, inflammatory bowel disease and others. There is also some recent evidence that fish oil derived resolvins inflammatory conditions such as severe gum disease, which lipoxins from arachidonic acid is not present. These new data indicate that PUFA fish oil can have a unique anti-inflammatory action under certain conditions of disease. * For more information, see Government publications. .