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Lipid mediators


Also listed as: WAS
Related terms
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Prostaglandins (pgs)

Related Terms
  • Antibodies, auto recessive, B-cells, bone marrow, bone marrow transplant, CBC, genetic disorder, immune system, immunodeficiency, inherited disorder, inherited immunodeficiency, leukocytes, leukemia, lymphoma, lymphocytes, malignancy, platelets, pneumonia, red blood cells, T-cells, thrombocytes, thrombocytopenia, tumor, WASP, white blood cells, Wiskott Aldrich syndrome, Wiskott-Aldrich syndrome protein, X-linked.

  • Wiskott-Aldrich syndrome (WAS) is an inherited, immunodeficiency disorder that occurs almost exclusively in males. The recessive genetic disorder is caused by a mutation in the WAS (Wiskott-Aldrich syndrome) gene, which is an X-linked trait. The gene mutation leads to abnormalities in B- and T-lymphocytes (white blood cells), as well as blood platelet cells. In a healthy individual, the T-cells provide protection against viral and fungal infection, the B cells produce antibodies, and platelets are responsible for blood clotting to prevent blood loss after a blood vessel injury.
  • Individuals diagnosed with WAS suffer from recurrent infections, eczema and thrombocytopenia (low levels of platelets).
  • Before 1935, patients only lived an average of eight months. Today, patients usually live an average of eight years, according to a recent case study. The cause of death is usually attributed to extensive blood loss. However, cancer (especially leukemia) is common and often fatal among WAS patients.
  • The only possible cure for WAS is a bone marrow transplant. However, if a patient's family member is not a possible match for a bone marrow donation, patients may have to wait years for a potential donor. Other aggressive treatments may also increase a patient's life expectancy. For instance, one study found that patients who underwent splenectomy (removal of the spleen) lived to be more than 25 years old. The spleen may harbor too many platelets, and cause a decrease in the number of platelets in circulation. Antibiotics, antivirals, antifungals, chemotherapeutic agents, immunoglobulins and corticosteroids have also been used to relieve symptoms and treat infections and cancer associated with WAS.
  • Researchers estimate that about four people per one million live male births develop the disease in the United States.
  • The syndrome is named after Dr. Robert Anderson Aldrich, an American pediatrician who described the disease in a family of Dutch-Americans in 1954, and Dr Alfred Wiskott, a German pediatrician who discovered the syndrome in 1937. Wiskott described three brothers with a similar disease, whose sisters were unaffected.

Author information
  • This information has been edited and peer-reviewed by contributors to the Natural Standard Research Collaboration (

  1. Binder V, Albert MH, Kabus M, et al. The genotype of the original Wiskott phenotype. N Engl J Med. 2006 Oct 26;355(17):1790-3.
  2. Jin Y, Mazza C, Christie JR, et al. Mutations of the Wiskott-Aldrich Syndrome Protein (WASP): hotspots, effect on transcription, and translation and phenotype/genotype correlation. Blood. 2004 Dec 15;104(13):4010-9. Epub 2004 Jul 29.
  3. Natural Standard: The Authority on Integrative Medicine. .
  4. St. Jude Children's Research Hospital. Inherited Immunodeficiencies: Wiskott-Aldrich Syndrome (WAS). .
  5. U.S. Immune Deficiency Foundation. The Wiskott Aldrich Syndrome. .

Prostaglandins (pgs)
  • Ulf von Euler of Sweden discovered prostaglandins (PGs) and isolated them from human semen in the 1930s. It was initially believed that prostaglandins were produced in the prostate gland, which is why they were named prostaglandins. It has since been determined that prostaglandins are produced in nearly every cell in the body.
  • Prostaglandins are similar to hormones because they serve as chemical messengers. However, prostaglandins do not move to other places in the body. Instead, they work inside the cells where they are produced.
  • Prostaglandins activate the inflammatory response and produce symptoms of pain and fever in the body. When tissues become damaged, white blood cells migrate to the site to minimize tissue destruction and prostaglandins are produced to help stimulate cells involved in this response.
  • Different prostaglandins have different functions. For instance, when a blood vessel is damaged, a type of prostaglandin called thromboxane is released. This prostaglandin stimulates cells in the blood, called platelets, to form blood clots. This action reduces bleeding in the body and prevents further destruction.
  • Another type of prostaglandin, called PG12, has the opposite effect on thromboxane. PG12 is produced to stop blood clots from forming on the walls of blood vessels.
  • Other prostaglandins help induce reproductive processes, such as labor. For instance, PGE2 causes uterine contractions, which induces labor.
  • Prostaglandins are involved in several other organs as well. For instance, in the gastrointestinal tract, they inhibit the production of stomach acid and increase secretion of protective mucus. They also increase blood flow in the kidneys, which are responsible for filtering waste from the blood.
  • Drugs have been developed to inhibit prostaglandins from acting. For instance, nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Motrin®, Advil®), block an enzyme called cyclooxygenase (COX), which is involved in the production of prostaglandins. Blocking the COX enzyme prevents prostaglandins from being produced and subsequently relieves symptoms of pain and fever.

  • Swedish biochemist Bengt Samuelsson first discovered leukotrienes in 1979. These mediators were first discovered in white blood cells derived from bone marrow (leukocytes).
  • Leukotrienes are inflammatory molecules that exhibit a wide range of biological activities, most of which involve sending signals or messages to other cells in the body.
  • There are two main types of leukotrienes: leukotriene B4 and cysteinyl leukotrienes. Leukotriene B4 is involved in inflammatory conditions that are dependent on white blood cells called neutrophils. When these leukotrienes are released into the blood, they signal neutrophils to move towards the site of injury in the body. Leukotriene B4 has also been associated with long-term conditions, such as cystic fibrosis, inflammatory bowel disease (IBD), and psoriasis.
  • Inflammatory cells called eosinophils and mast cells produce cysteinyl leukotrienes. When cysteinyl leukotrienes are produced, they signal more eosinophils and/or mast cells to move towards the site of injury in the body. These leukotrienes have also been associated with asthma and allergies.
  • Cysteinyl leukotrienes are one of severalsubstances that are released by mast cells during an asthma attack. These leukotrienes signal more mast cells to migrate toward the area causing the airway muscles to contract and mucus secretion to increase. As a result, the airways narrow and symptoms of asthma, including difficulty breathing and wheezing, occur. Long-term cases of asthma appear to be caused by inflammatory cells called eosinophils, which also release cysteinyl leukotrienes. Therefore, leukotrienes are capable of triggering both short-term asthma attacks and long-term asthma symptoms.
  • Drugs have been developed to prevent leukotrienes from having negative effects on the body. For instance, both leukotriene synthesis inhibitors, such as zafirlukast (Accolate®), and cysteinyl-leukotriene receptor antagonists, such as montelukast (Singulair®) and zileuton (Zyflo®), have been shown to prevent asthma attacks in asthmatic patients. However, these drugs are not effective treatments once the asthma attack has started.
  • Leukotriene synthesis inhibitors prevent mast cells or eosinophils from releasing leukotrienes. Cysteinyl leukotriene receptor antagonists block specific leukotriene receptors on bronchial tissues in the airway, which subsequently prevents the airway constriction, mucus secretion, and inflammation. Cysteinyl leukotriene receptor antagonists also reduce the influx of eosinophils, which reduces inflammatory damage in the airways.

  • Lipoxins (LXs) are anti-inflammatory mediators. Unlike prostaglandins and leukotrienes, the lipoxins signal the resolution of inflammation.
  • Once the injurious stimulus, such as bacteria, has been removed from the body, destroyed, or broken, lipoxins are released to stop the inflammatory response. When lipoxins are released, the white blood cells are no longer signaled to move toward the site of injury. As a result, inflammation in the body decreases.

Copyright © 2011 Natural Standard (

The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.

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