Crohns recipes can play an important role in preventing Crohn’s symptoms or flare ups, regardless if a person suffers from Crohn’s ileitis or another form. It is no secret that the food a person ingests can have positive or negative affects on their digestive system and gastrointestinal tract.

However, just because a person with Crohn’s has to watch what they eat, and omit various food products from their diet, doesn’t mean they can’t enjoy the foods they eat. The following are five foods that are generally considered safe for a Crohns recipes diet and can provide extra nutrition and/or flavour.

1. Honey – Honey is a natural sweetener that has healing properties. It is a good source of antioxidants and is ideal for treating diarrhea, as it encourages rehydration in the body and soothes the stomach. In addition, honey has free sugar molecules which actually improves brain function and reduces fatigue.

It is imperative that you purchase local raw honey to ensure you are receiving all of its nutrients and enzymes in your crohns recipes. The best place to look for this honey is in health stores.

Recipe tips – Honey is perfect for sweetening your tea and other beverages. Also consider using honey as spread for your bread, and as an alternative to sugar required in certain recipes.

2. Coconut oil – Coconut oil contains a significant amount of lauric acid. This acid is easy to digest, and also works to strengthen the immune system, allowing protection against bacterial, viral and fungal infections.

In addition, Coconut oil detoxifies the liver, and aids in building fats, lipoproteins, bile and hormones which are needed for digestion; thus creating a healthy digestive tract. Coconut oil encourages the absorption of food nutrients, and speeds up metabolism.

Recipe tips: Use coconut oil for cooking. Use coconut oil as the substitute in crohns recipes that call for margarine, butter or other unhealthy oils. In addition, when left in room temperature, virgin coconut oil solidifies and can be used as a spread for bread in place of butter or margarine.

3. Soy Products – Soy products such as soy milk, soy burgers, soy meats, and soy cheese, tempeh and tofu, are excellent sources of protein and are ideal replacements for dairy. Some believe soy helps to reduce bowel inflammation associated with Crohn’s disease.

Recipe tips: Soy products come in many forms such as meats, burgers, cheese and milk. By substituting regular meat and dairy products for soy, and including dark leafy green vegetables, you can enjoy the meals you’ve always liked, and still obtain the nutrients you need. Try adding soy milk or soy vanilla milk to cereal, in tea or fruit smoothies, and top off your salad with soy cheese.

4. Extra Virgin Olive Oil - Extra virgin olive oil is vegetable based and an excellent addition to crohns recipes. This oil helps to protect your intestines as it contains potent antioxidants. Olive oil also increases the body’s absorption of a number of vitamins including A, D, E, and K. Furthermore, it encourages faster healing and increases metabolism.

Recipe tips: Olive oil is a flavor enhancer and is a fantastic alternative to margarine or butter for recipes and as condiment. For instance, you can use it as a salad dressing.

5. Essential Fatty Acid Foods – Be sure to spice up your recipes with foods that are high in essential fatty acids, as they are known to prevent inflammation within the bowel. Good sources of such foods include dark green leafy vegetables, rapeseed, walnuts and flaxseed.

Recipe tips: Introduce salad to your diet, and don’t be afraid to add nuts and seeds to recipes. For instance, if you have a cookie recipe you love, add some walnuts.

Remember, not everyone’s Crohn’s symptoms are triggered by the same foods. Therefore, make sure you find out what foods aggravate your condition, so you can avoid them. If you are having a difficult time finding crohns recipes that work for you, it’s a good idea to take your concerns and questions to a qualified dietitian who can help you find answers, and start you on a diet that works for you.

About the author: Grab your free copy of Sharon Dobson’s brand new Crohn’s Disease Newsletter - Overflowing with easy to implement methods to help you discover more about acupuncture and crohns

You need to know about cholesterol triglyceride because it is this cholesterol that will cause give you a variety of cardiovascular diseases. Triglycerides are part of the cholesterol picture that is not talked about very much and are extremely dangerous for your health. And, they come from the fat that you eat every day.

Cholesterol triglyceride is a lipid, which is a type of fat. This fat is used by every body cell in its membrane structure and in your brain. When cholesterol triglyceride combines with protein a new chemical is created called “lipoproteins”, which flows through your blood.

As lipoproteins circulate in your arteries, they tend to deposit their fat on your artery walls. This process is always occurring, but the problem is when you have high cholesterol triglyceride you create high lipoproteins. The result is you deposit more fat on your artery walls than normal.

Clinical studies show that people with high cholesterol triglyceride are more prone to heart disease. So why don’t you hear about triglyceride instead of just HDL and LDL cholesterol. The reason is that there aren’t any drugs that can lower cholesterol triglyceride, so doctors don’t often discuss this part of the cholesterol picture.

So to reduce your susceptibility for heart disease, you need to reduce your cholesterol triglyceride. How do you know if yours is high? You need a blood test and need to talk with a doctor about your results.

Here is a list of some of the damage high cholesterol triglyerides can do:

At 200 ml/dl your risk for coronary artery disease doubles

At 200 ml/dl and HDL less than 40 mg/dl your risk for coronary artery disease is four times greater.

At 200 ml/dl women have a higher risk of artery disease than men

If you have diabetes, you are more prone to higher triglyceride levels

High triglyceride levels make you prone to kidney and pancreas diseases

Now, to have lower triglyceride levels, you can change some of your diet habits. I always recommend you change them gradually as you learn about good eating habits..

Here are two ways to control triglyerides:

Exercise regularly – the way you exercise makes a difference on your cholesterol triglyceride level. Instead of a straight 30 minutes brisk exercise do three 10 minutes brisk exercises during the day. By adding some resistive exercise, you gain more benefits for your heart and bones.

Diet - Eat a balanced diet that’s low in sugar, simple carbohydrates, and processed foods. Eat more fruits and vegetables to get the fiber. Fiber will help you keep your cholesterol triglyerides low. Fiber will trap excess cholesterol as it is released into the colon through your gallbladder and moved out in your stools. The less fiber there is in the colon the more cholesterol is reabsorbed back into the body through your colon walls.

There you have it, concentrate your efforts on keeping your cholesterol triglyerides low by eating less processed fats, less processed foods, exercising throughout the day, and eating more fiber.

Bio:

Over the years, researchers have stipulated that green or black tea consumption reduces the risk of cardiovascular disease. This is very important because people from all walks of life inevitably suffer from some form of this potentially deadly disease.

According to the American Heart Association, in 2003, there were 71,300,000 individuals that have this disease and it claimed 910, 614 lives that year alone. This disease does not just affect people in the United States. It also affects international residents. In the U.K alone, cardiovascular disease was responsible for over 23,000 deaths in 2004. In other words, every one (regardless of where they live) is at risk for this potentially deadly disease.

With this in mind, researchers have been working diligently to combat this illness. Numerous epidemiologic studies have indicated that consumption of green or black tea reduces the risk of cardiovascular disease. However, many are left wondering “How?”.

Scientists have made many assumptions about how these eas positively affects cardiovascular disease and research is still pending. One hypothesis states that drinking green or black tea affects lipoproteins. However, researchers have found that drinking green or black tea does not increase the resistance of low-density lipoprotein to oxidation in humans or the serum lipid concentrations in humans either.

Researchers determined this during a four week long parallel study comprising of 45 volunteers. The study involved the subjects drinking 900 ml (6 cups) of mineral water, black tea, or green tea daily. Blood samples were dutifully collected from the fasting subjects, both before and after the study. An in vitro experiment was carried out to record the effect of adding tea extract to plasma and the consequence on the resistance of isolated LDL to oxidation.

Data was carefully evaluated utilizing various research methodologies and researchers concluded that the said 900 ml (6 cups) of the beverage did not have any substantial effect on either serum lipid concentrations or resistance of LDL to oxidation. However, It was determined that the large intake of green tea did increase the total antioxidant activity of the plasma slightly.

Nevertheless, the arresting effect of tea flavonoids on cardiovascular disease is an open proposition and researchers are still evaluating other probable mechanisms. For instance, many researchers stipulate that green or black tea may have a positive effect on the panacea and on cardiovascular disease.

Before we discuss this hypothesis further, let’s take a moment to discuss how cardiovascular disease is triggered. In some cases, cardiovascular disease runs in families, and in other cases it doesn’t. Many of its victims experience such triggers like high cholesterol, raised blood pressure, and obesity. In addition, stress is thought to contribute to this disease.

As such, physicians currently prescribe a preventive diet of fruits, vegetables, nuts, and Omega 3 fatty acids in order to keep this disease at bay. In addition, physicians also recommend that patients engage in regular exercise, reduce stress and anxiety levels, and quit smoking to help prevent and keep CVD in check. In addition, drinking black or green tea is also an important addition on the list. However, it is still unclear the extent to which tea helps control CVD, but researchers are not giving up.

Animal and in vitro studies have suggested numerous and probable cardiovascular protective mechanisms of tea which include prohibition of oxidized LDL cholesterol, the disintegration of the inflammatory process in atherosclerosis, reducing thrombosis, promotion of normal endothelial function, reduction of total plasma, and LDL cholesterol and adhesion molecules blocking mechanisms.

In addition, the effect of tea consumption on platelet aggression shows mixed results. A study by Duffy, et al. noted an improved endothelial function post consumption of black tea. In addition, researchers believe that green or black tea also positively effect endothelial function and have found that polyphenolic compounds in tea other than catechins are responsible for improved endothelial function in humans.

Blood pressure is another area where the cardio-protective properties of tea are believed to have a positive influence. However, studies have shown that a positive effect is seen among subjects who had been drinking tea for at least a year, if not more. Short-term tea drinking has not made much of a difference.

Cholesterol comes in two sizable forms and it is essential to not only conceive the divergence between the two forms, but also cognize the types of foods that swell “positive” cholesterol while lowering “bad” cholesterol. Only through such discernment can you choose a diet that can lower your risk of developing coronary heart sickness and help counter a heart attack or stroke.

HDL versus LDL Cholesterol

Cholesterol does not dissolve in the blood, it must be transported by lipoproteins to and from the cells within the body. HDL, or “agreeable” cholesterol is high-priced density lipoprotein and it carries up to 1/3 of the blood cholesterol throughout the body. HDL is considered “valuable” cholesterol because excessive levels of HDL have been shown to guard against heart affliction and heart attack. LDL, on the other hand, is considered to be “bad” cholesterol. When indulgent amounts of low density lipoprotein are in the blood, it can aggregate within the inner walls of the arteries over time and form plaque that can restrict blood flow through the arteries.

What Are The Sources of Cholesterol?

The cholesterol in your bloodstream comes from both the food you eat as well as naturally from your own body. Nearly 75 percent of the cholesterol located in your blood is produced by your liver and other cells within your body while the other 25 percent comes from the food you eat. LDL, or “bad” cholesterol, is produced naturally by the body, but hereditary elements may determinent your body to produce too much of the cholesterol. This is why it is relevant to make nourishing dietary choices to greater regulate the 25 percent of cholesterol production that comes from food.

What Foods Can We Avoid?

Food expensive in saturated and Trans fats: Avoid eating food stiff in saturated and trans fats. Read food labels to ascertain the quantity of saturated and trans fats they comprise. These labels will a remedy you avoid foods steep in fat and allow you to choose more nourishing alternatives. Also look for foods with the heart-check dwight symbol on their label. This label indicates that the food is approved by the American Heart Association as part of a energy-giving diet.

(NO! Not the ice cream!!) Whole fat dairy products: Avoid whole fat dairy products such as whole milk, butter, full-fat cheese and yogurt. If possible, substitute them with fat-free, reduced-fat or low-fat dairy products.

Foods stiff in dietary cholesterol: Avoid foods exorbitant in dietary cholesterol including whole eggs, shellfish, and organ meats. Compensate whole eggs with egg whites and organ meats with lean meats. As a goal, try to limit your intake of cholesterol to secondary than 300 mg a day.

Which Foods Lower “Bad” Cholesterol?

Almonds and walnuts: Almonds and walnuts have been shown to lower LDL, or “bad” cholesterol. Just about a handful of almonds or walnuts a days can significantly lower your cholesterol levels

while improving the health of your blood vessels.

Foods with soluble fiber: Oatmeal encompasses soluble fiber that can lower LDL, or “bad” cholesterol, while keeping HDL, or “agreeable”

cholesterol, equable. Additional foods containing soluble fiber include apples, pears, barley and rice.

Foods with omega 3 fatty acids: Fish takes in omega 3 fatty acids which have been shown to lower LDL while raising HDL cholesterol.

Recommended fish with omega 3 fatty acids include salmon, sardines, albacore tuna and mackerel. Food other than fish containing omega 3 fatty acids include canola oil, flaxseed and soybean oil.

How Can I Prepare My Befitting Diet?

Begin by determining your dietary goals. Do you need to lower your cholesterol considerably or only slightly? Do you yearn to lose weight at the same time as you lower your cholesterol? Will this be a short-term dietary change or a replete standing change?

Only once you know your goals can you properly plan your new diet plan and begin to lower your bad cholesterol and dwindle your risk of heart disease.

Lower Cholesterol Naturally And Safely With Red Rice Yeast

It is possible to lower cholesterol safely and naturally by using red rice yeast, but before you consider doing so you should be aware of what cholesterol is and what it does to your body. It is, in fact, an oily liquid that is essential for your bodys health. You cannot do without it. Why then are people telling you that it is bad for you?

Lets have a closer look at cholesterol, then, and try to resolve this paradox. Cholesterol is needed to make cell membranes and also some hormones and other components your body needs, and the main transportation system used is the bloodstream and its network of pipes leading all parts of the body. Because the blood is aqueous, and cholesterol is an oil, they do not mix. In order for the cholesterol to be transported to the parts of your body where it is needed, it uses a transport system, a bit like a taxicab.

The cabs used by cholesterol are called lipoproteins, which carry cholesterol and other fats around your body. There are a number of different kinds of lipoprotein, but the two we are concerned about are low density lipoprotein (LDL) and high density lipoprotein (HDL). Low density lipoprotein is the main cholesterol carrier in your blood, and if too much cholesterol carried by LDL circulates rounds the blood, cholesterol deposits can build up on the artery walls of your heart and brain.

This can eventually build up into a hard lining called plaque, and eventually effectively narrow the arteries. This reduces the blood flow, and is called atherosclerosis, or hardening of the arteries. If these are coronary arteries it is called coronary artery disease, and you are at increased risk of a heart attack. If they are arteries in the brain, they are called cerebral vascular disease, and you are at risk of having a stroke. Either of these two serious effects can result in death, and can be caused by a blood clot.

An LDL cholesterol level of 160 mg/dl (milligrams/deciliter) is very dangerous, and if you have heart problems your cholesterol level should be below 100. However, about a third to a quarter of your bodys cholesterol content is carried by high density lipoproteins, that are believed to carry cholesterol from the blood to the liver where it is processes and expelled from the body. A high level of HDL cholesterol is therefore good for you and a low level of HDL in your body (less than 40 mg/dl for men and 50 for women) can also be dangerous.

You ingest cholesterol from animal sourced foods, such as meats, eggs and dairy products. Fruits and vegetables contain none. However, the liver produces about 1 gram (1000 mg) of cholesterol a day, while you consume only 150 200 mg from your diet. An American male can consume an average of around 340 mg per day, while it should be limited to below 300. Saturated fatty acids and trans fats are responsible for the bodys cholesterol production, and you can get these from vegetarian as well as animal sources.

So how can you reduce your cholesterol? You can get prescription medicines such as statins, bile acid sequestrants and fibrates, but all have some effect on your liver. They generally work by requiring your liver to use up cholesterol to make up for deficiency created by the drug, or by creating less LDL cholesterol, so an overdose can be very dangerous and all of them have specific side effects that you should ask your doctor about. Statins might also need an enzyme supplement since they can deplete the enzyme Co-Q10 that can lead to heart problems. You must ask your doctor about this.

A natural treatment for high LDL cholesterol levels is red rice yeast. This is produced by fermenting of red yeast called Monascus purpureus over rice. It is what gives Peking duck its characteristic red coloring, and is used in other forms of Chinese cookery. It is also a traditional Chinese remedy for indigestion, diarrhea and poor circulation, and contains a natural statin called lovastatin that inhibits the production of an enzyme that promotes the production of cholesterol by the liver.

Unfortunately, when the FDA found that the red rice yeast contained lovastatin, it insisted it be recalled since it contained an uncontrolled pharmaceutical ingredient. There is now an ongoing legal battle about whether red rice yeast is a pharmaceutical drug or a dietary supplement. The rice is still commonly sold.

However, due to the unclear legal situation the rice containing lovastatin can still be purchased online, and studies have shown it to significantly lower LDL cholesterol when compared to a placebo. The mevinolin that contains the lovastatin is a natural product, occurring naturally in red rice yeast, and lovastatin is not the only active ingredient. If you decide to try it, make sure that you are not using any other cholesterol treatments at the same time, and that you have no existing liver condition.

Like statins, it works by reducing the Coenzyme Q-10 reductase content of your body, which reduces the need for the liver to produce cholesterol. However, some studies have shown that red rice yeast is more effective that pharmaceutical statins and reduces cholesterol by a greater amount with fewer health problems. However, like all natural remedies that are taken for serious conditions, your physician might have the last say.

There is still a considerable debate being carried out on the effects of cholesterol on the body, with both camps firmly entrenched. However, the bulk of scientific and medical evidence suggests that too high a LDL cholesterol level in the blood can lead to artherosclerosis, and there is no debating the effects of that condition! It is safer to reduce your cholesterol level than to let it be, and a natural means of doing that must be better than using prescription drugs.

red rice yeast has been shown to be effective and the Chinese have yet to be shown to have suffered the predicted side effects of statins. However, as with any cure for a serious condition, the patient should be aware of the potential problems and their symptoms, and consult their doctor before taking any remedy.

Toll-Like Receptor(TLR) : Unique Antibody from Imgenex

Toll-like receptor (TLR) family is a phylogenetically conserved mediator of innate immunity that is essential for microbial recognition. TLRs are evolutionarily conserved and their congeners have been found in insects, plants, and mammals. Drosophila Toll (dToll) was the first member of the TLR family to be identified, and was initially characterized as a developmental protein governing the formation of the dorsal-ventral axis in Drosophila. Mammalian TLRs represent a growing family of transmembrane proteins characterized by multiple copies of leucine-rich repeats (LRRs) in the extracellular domain and a cytoplasmic Toll/IL-1R (TIR) motif and therefore, TLRs are thought to belong to the IL-1R superfamily. Recently, TLRs were observed to influence the development of adaptive immune responses, presumably by activating antigen-presenting cells. To sense innumerable and various pathogenic threats, TLRs have evolved to recognize pathogen-associated molecular patterns (PAMPs), which represent molecular features on the surface of pathogens. Each TLR binds to a variety of PAMPs that work as molecular markers of potential pathogens that the host shall be defended against. So far, 11 members of the TLR family (TLR1-TLR11) have been identified in mammals. TLR1, TLR2, TLR6, TLR4, and TLR5 are located on the plasma membrane, whereas TLR3, TLR7, and TLR9 are not located on the cell surface. TLR2 is involved in the responses to a variety of bacterial components that include peptidoglycan, lipoproteins/ lipopeptides, glycosyl-phosphatidylinositol anchors from Trypanosoma cruzi, and zymosan. Flagellin, a potent pro-inflammatory inducer, is recognized by TLR5. TLR3 recognizes dsRNA, a viral product, whereas TLR9 recognizes unmethylated CpG motifs frequently found in the genome of bacteria and viruses, but not vertebrates. TLR7 recognizes the pharmaceutical compounds imiquimod (also known as Aldara, R-837 or S-26308) and resiquimod (also known as R-848 or S-28463). It has recently been shown that TLR11, which is abundant in the kidney and bladder, senses uropathogenic bacteria. They are usually classified into three subgroups.. Members of subgroup 1 bind interleukins that are produced by macrophages, monocytes and dendritic cells and all have Immunoglobulin (Ig) domains. Members of subgroup 2 bind directly pathogen-associated molecules (LPS, peptidoglycan etc.). A third subgroup consists of adaptor proteins that are exclusively cytosolic. The toll-like receptor (TLR) signaling pathway is the front-line subsystem against invasive microorganisms for both innate and adaptive immunity and has been evolutionarily well conserved in both invertebrates and vertebrates.Reference: 1. A comprehensive map of the toll-like receptor signaling network. Molecular Systems Biology Article number: 2006.0015 . Kanae Oda %26 Hiroaki Kitano2. Toll-like receptor downstream signaling Taro Kawai and Shizuo Akira Arthritis Res Ther. 2005; 7(1): 12–19.3. A Toll-like receptor recognizes bacterial DNA Nature 408, 740-745 (7 December 2000) Hiroaki Hemmi, Osamu Takeuchi, Taro Kawai, Tsuneyasu Kaisho, Shintaro Sato, Hideki Sanjo, Makoto Matsumoto, Katsuaki Hoshino, Hermann Wagner, Kiyoshi Takeda and Shizuo Akira.

TLR2- cluster of differentiation 282

Toll-like receptor 2 (TLR2), often designated as CD282 (cluster of differentiation 282) is a type I transmembrane protein belonging to the large homologous family of Toll like receptors. TLR2 acts as functional receptor for both Gram-positive and Gram-negative bacteria. Like all other members of the TLR family, TLR2 is composed of an extracellular domain containing multiple leucine-rich repeats (LRRs), a transmembrane region, and a cytoplasmic tail containing the conserved TIR domain. TLR2 maps to chromosome 4q31-32 and encodes a putative 784 amino acid protein with 19 N-terminal LLRs and a calculated molecular weight of 84 kDa (1, 2, 3). Comparison of the amino acid sequence reveals that TLR2, TLR1, and TLR6 form a TLR subfamily, which presumably diverged from one common ancestral gene. In humans, TLR10 is also a member of this TLR2 subfamily. Among all TLR, TLR1 and TLR6 have the highest identity of overall amino acid sequence, which is 66%, and a similar genomic structure and thus it is assumed that they are the evolutionary products of gene duplication. In vivo transcripts for TLR2 are observed suggesting that the mRNA is alternatively spliced. TLR2 mRNA expression is observed in brain, heart, lung, and spleen tissues and is highest in PBLs, specifically those of myelomonocytic origin. In vitro PMA-differentiated THP-1, TLR2 is most significantly upregulated by autocrine IL-6 and TNF-α, IL-1β, and IL-10. Further, TLR2 mRNA expression is elevated after exposure to both Gram-positive and Gram-negative bacteria. The increase in TLR2 expression in monocytes and granulocytes on exposure to Gram-negative bacteria is only very modest. Furthermore, TLR2 appears to be up-regulated on mononuclear cells during disorders such as chronic obstructive pulmonary disease, influenza virus infections, and sepsisTLR2 act as signal transducers for various bacterial components which include lipoproteins derived from M. tuberculosis, Borrelia burgdorfei, Treponema pallidium and Mycoplasma fermentans. In addition, TLR2 mediates cellular responses to a wide variety of infectious pathogens and their products which include yeast cell walls, whole mycobacteria, mycobacterial ara-lipoarabinomannan, whole Gram-positive bacteria, peptidoglycan (PGN), Treponema glycolipid and Trypanosoma cruzi glycophosphatidylinositol anchor. TLR2 forms heterodimers with TLR1, TLR6 and possibly TLR10, where each complex is particularly sensitive to subsets of TLR2-associated pathogen-associated molecular patterns (PAMPs). It has been studied that TLR6 and TLR2 function together to detect Gram-positive bacteria, PGN and zymosan, whereas TLR2 functions either alone or with TLRs other than TLR6 to detect bacterial lipopeptides. More recent studies have suggested that, like TLR4, TLR2 complexes require CD14 and MD-2 for detection of PAMPs and signaling. (4, 5) Upon ligand recognition, TLR2 recruits both the TIR domain-containing sorting adaptor TIRAP and the signaling adaptor MyD88, and initiates the MyD88-dependent pathway. The MyD88-dependent pathway activates nuclear factor (NF)-κB, activator protein-1 (AP-1) and interferon regulatory factor 5 (IRF5), which induce inflammatory cytokine expression such as IL-6, IL-12, and TNFα. (6)Aside from detection of non-self patterns, TLR2 complexes are also capable of detecting altered self patterns, such as those displayed by necrotic cells. Further, recent evidence indicates that TLR2 is recruited to phagosomes and may be directly involved in the internalization of microbial products by cells.Reference:1. Rock, F.L. et al. (1998) Proc. Natl. Acad. Sci. USA 95:588.2. Chaudhary, P.M. et al. (1998) Blood 91:4020.3. Dunne, A. %26 L.A.J. O’Neill (2003) Sci. STKE 2003:re3.4. Modlin, R.L. (2002) Ann. Allergy Asthma Immunol. 88:543.5. J Endotoxin Res. 2000;6(5):401-56. Annual Review of Biochemistry Vol. 76: 447-480 (Publication date July 2007)

TLR2- cluster of differentiation 282

Toll-like receptor 2 (TLR2), often designated as CD282 (cluster of differentiation 282) is a type I transmembrane protein belonging to the large homologous family of Toll like receptors. TLR2 acts as functional receptor for both Gram-positive and Gram-negative bacteria. Like all other members of the TLR family, TLR2 is composed of an extracellular domain containing multiple leucine-rich repeats (LRRs), a transmembrane region, and a cytoplasmic tail containing the conserved TIR domain. TLR2 maps to chromosome 4q31-32 and encodes a putative 784 amino acid protein with 19 N-terminal LLRs and a calculated molecular weight of 84 kDa (1, 2, 3). Comparison of the amino acid sequence reveals that TLR2, TLR1, and TLR6 form a TLR subfamily, which presumably diverged from one common ancestral gene. In humans, TLR10 is also a member of this TLR2 subfamily. Among all TLR, TLR1 and TLR6 have the highest identity of overall amino acid sequence, which is 66%, and a similar genomic structure and thus it is assumed that they are the evolutionary products of gene duplication. In vivo transcripts for TLR2 are observed suggesting that the mRNA is alternatively spliced. TLR2 mRNA expression is observed in brain, heart, lung, and spleen tissues and is highest in PBLs, specifically those of myelomonocytic origin. In vitro PMA-differentiated THP-1, TLR2 is most significantly upregulated by autocrine IL-6 and TNF-α, IL-1β, and IL-10. Further, TLR2 mRNA expression is elevated after exposure to both Gram-positive and Gram-negative bacteria. The increase in TLR2 expression in monocytes and granulocytes on exposure to Gram-negative bacteria is only very modest. Furthermore, TLR2 appears to be up-regulated on mononuclear cells during disorders such as chronic obstructive pulmonary disease, influenza virus infections, and sepsisTLR2 act as signal transducers for various bacterial components which include lipoproteins derived from M. tuberculosis, Borrelia burgdorfei, Treponema pallidium and Mycoplasma fermentans. In addition, TLR2 mediates cellular responses to a wide variety of infectious pathogens and their products which include yeast cell walls, whole mycobacteria, mycobacterial ara-lipoarabinomannan, whole Gram-positive bacteria, peptidoglycan (PGN), Treponema glycolipid and Trypanosoma cruzi glycophosphatidylinositol anchor. TLR2 forms heterodimers with TLR1, TLR6 and possibly TLR10, where each complex is particularly sensitive to subsets of TLR2-associated pathogen-associated molecular patterns (PAMPs). It has been studied that TLR6 and TLR2 function together to detect Gram-positive bacteria, PGN and zymosan, whereas TLR2 functions either alone or with TLRs other than TLR6 to detect bacterial lipopeptides. More recent studies have suggested that, like TLR4, TLR2 complexes require CD14 and MD-2 for detection of PAMPs and signaling. (4, 5) Upon ligand recognition, TLR2 recruits both the TIR domain-containing sorting adaptor TIRAP and the signaling adaptor MyD88, and initiates the MyD88-dependent pathway. The MyD88-dependent pathway activates nuclear factor (NF)-κB, activator protein-1 (AP-1) and interferon regulatory factor 5 (IRF5), which induce inflammatory cytokine expression such as IL-6, IL-12, and TNFα. (6)Aside from detection of non-self patterns, TLR2 complexes are also capable of detecting altered self patterns, such as those displayed by necrotic cells. Further, recent evidence indicates that TLR2 is recruited to phagosomes and may be directly involved in the internalization of microbial products by cells.Reference:1. Rock, F.L. et al. (1998) Proc. Natl. Acad. Sci. USA 95:588.2. Chaudhary, P.M. et al. (1998) Blood 91:4020.3. Dunne, A. %26 L.A.J. O’Neill (2003) Sci. STKE 2003:re3.4. Modlin, R.L. (2002) Ann. Allergy Asthma Immunol. 88:543.5. J Endotoxin Res. 2000;6(5):401-56. Annual Review of Biochemistry Vol. 76: 447-480 (Publication date July 2007)