Interleukin information and medical benefits and review of danger and risk
How to lower levels naturally

January 6 2017 by
Ray Sahelian, M.D.

Interleukins are a group of cytokines that were first noticed to be released by white blood cells (leukocytes, hence the -leukin) as a means of communication, hence the term 'inter.' Further research indicated that interleukins are made by a wide variety of bodily cells. There are many types of interleukins, and they are numbered as interleukin 1, 2, etc.

Diet and interleukin production
Increased intakes of dietary alpha linolenic acid elicit antiinflammatory effects by inhibiting interleukin 6, interleukin 1 beta, and TNF-{alpha} production in cultured peripheral blood mononuclear cells. Changes in PBMC alpha linolenic acid and eicosapentaenoic acid (derived from dietary ALA) are associated with beneficial changes in TNF-{alpha} release. Thus, the cardioprotective effects of alpha linolenic acid are mediated in part by a reduction in the production of inflammatory cytokines.

Interleukin and food allergy
Interleukin-12 may protect against food allergies. A British team at the Institute of Food Allergy Research in Norwich noted that interleukin-12 is absent during the body's allergic response. "We have identified a molecule that is very important for the regulation of immune response and for the first time clearly represents a potential target for the therapy of allergy. This is currently under investigation," lead researcher Claudio Nicoletti said in a prepared statement. The Interleukin-12 molecule is made by white blood cells. These cells help regulate the body's immune response to foreign materials, including food proteins. Researchers compared cells in the gut and spleen of mice with and without food allergies. Cells in the allergic mice did not make interleukin-12. The discovery helps explain how "a food protein can be perfectly harmless to one person and lethal to another," Nicoletti said. "We have identified the missing molecule that normally keeps immune responses under control." July 2007 issue of the Journal of Allergy and Clinical Immunology.

Asthma treatment
Lancet. 2015. Targeting the interleukin pathway in the treatment of asthma. Current therapies based on inhaled corticosteroids and longacting β2 agonists are effective in controlling asthma in most, but not all patients, with a few patients falling into the severe asthma category. Severe asthma is characterised by poor asthma control, recurrent exacerbations, and chronic airflow obstruction despite adequate and, in many cases, high-dose treatments. There is strong evidence supporting the role for interleukins derived from T-helper-2 (Th2) cells and innate lymphoid cells, such as interleukins 4, 5, and 13, as underlying the eosinophilic and allergic inflammatory processes in nearly half of these patients. An anti-IgE antibody, omalizumab, which binds to circulating IgE, a product of B cells from the actions of interleukin 4 and interleukin 13, is used as treatment for severe allergic asthma. Studies examining cytokine blockers such as anti-interleukin-5, anti-interleukin-4Rα, and anti-interleukin-13 monoclonal antibodies in patients with severe asthma with recurrent exacerbations and high blood eosinophil counts despite use of inhaled corticosteroids have reported improved outcomes in terms of exacerbations, asthma control, and forced expiratory volume in 1 s.

Interleukin 6, how to lower
Effects of quercetin on angiotensin II induced interleukin-6 in vascular smooth muscle cells
Zhong Yao Cai. 2006. Department of Pharmacology, Xi'an Jiao University of Medicine, China.
To observe the effects of quercetin on angiotensin induced interleukin-6 (IL-6) in vascular smooth muscle cells (VSMCs). VSMCs were isolated from the thoracic aorta of Sprague-Dawley rats and were stimulated with different doses of angiotensin II. The production of IL-6 in supernatant of quercetin treated cultures was detected by ELISA. In parallel, interleukin-6 mRNA level was measured by RT-PCR. angiotensin II induced a marked increase of interleukin-6 in a dose- and time-dependent manner in the culture of VSMCs. Quercetin inhibited the production of Ang II -induced interleukin-6 in the culture in a dose-dependent manner. Similarly, the result with RT-PCR indicated that the expression of interleukin-6 mRNA induced by angiotensin II for 24h was down-regulated by quercetin. It demonstrates that quercetin possesses a inhibition of angiotensin II-induced production of IL-6 in VSMCs. Moreover, quercetin also down regulates the expression of interleukin-6 mRNA, suggesting the action of quercetin on interleukin-6 release induced by angiotensin II in VSMCs may underlie its anti-inflammatory properties.

Plant Foods Hum Nutr. 2013. Role of maca herb (Lepidium meyenii) consumption on serum interleukin-6 levels and health status in populations living in the Peruvian Central Andes over 4000 m of altitude. Consumption of maca was associated with low serum IL-6 levels and in turn with better health status scores.

Biomed Res Int. 2014. Interleukin 6 and Rheumatoid Arthritis. Interleukin-6 (IL-6) is a representative cytokine featuring pleiotropic activity and redundancy. A transient synthesis of IL-6 contributes to host defense against infectious agents and tissue injuries by inducing acute phase reactions and immunological and hematopoietic responses. However, uncontrolled persistent production of IL-6 may lead to the development of several immune-mediated diseases. Rheumatoid arthritis (RA) is a chronic disease with joint and systemic inflammation resulting from immunological abnormalities and it has been found that IL-6 plays a key role in the development of this disease. Clinical trials in various parts of the world of tocilizumab, a humanized anti-IL-6 receptor antibody, have proved its efficacy and tolerable safety either as monotherapy or in combination with disease-modifying antirheumatic drugs. As a result, it is currently used as a first-line biologic for the treatment of moderate-to-severe RA in more than 100 countries. Clarification of the mechanism(s) through which tocilizumab exerts its effect on RA and of the reason(s) why IL-6 is continuously produced in RA can be expected to lead to the best use of this agent for RA patients and aid in investigations into the pathogenesis of RA.

Interleukin 7 and HIV AIDS
Dr. Paolo Lusso and colleagues at the National Institutes of Health, National Institute of Allergy and Infectious Diseases looked at the role played by interleukin 7 in averting the death of T cells, a kind of white blood cell important to the immune system.  They used blood samples from 24 HIV-infected people. They added interleukin 7 to the blood samples and then gauged the survival of T cells. Interleukin 7 is a substance important in maintaining proper functioning of the immune system. The actual patients themselves were not treated with interleukin 7. The samples with interleukin 7 displayed lower levels of T cell death. The benefits differed from sample to sample based on the person's stage of infection. The researchers believe interleukin 7 potentially could be used alongside existing AIDS drugs to bolster the immune system. Existing AIDS drugs can keep the virus at bay for years, but damage to the immune system commonly persists even after years of such treatment. The next step is a study in which monkeys with the simian equivalent of HIV are given interleukin 7 to see if it blocks immune system dysfunction and immune cell depletion.

Interleukin 10
Int Immunopharmacol. 2015. Melatonin enhances interleukin-10 expression and suppresses chemotaxis to inhibit inflammation in situ and reduce the severity of experimental autoimmune encephalomyelitis.

Interleukin 23 and stroke
Akihiko Yoshimura at Keio University's School of Medicine in Tokyo, says that while the initial damage from a stroke cannot be prevented, drugs or medications can be used to limit secondary damage caused by immune cells that rush to the site of the infarction, or stroke. After the neural damage, macrophages and T-cells (two types of immune cells) are imported and this inflammation induces the growth of the infarction. One of the first groups of substances to enter the brain is called interleukin-23 (IL-23). "IL-23 itself is not harmful, but it activates other immune cells like T-cells and macrophages and these attack the brain. Nature Medicine, advance online publication August 2, 2009.

Dear Healthcare Provider: The purpose of this letter is to inform you of important safety information for ACTEMRA (tocilizumab), a new interleukin-6 (IL-6) receptor inhibitor that has been approved by the Food and Drug Administration (FDA) for the treatment of adult patients with moderately to severely active rheumatoid arthritis (RA) who have had an inadequate response to one or more tumor necrosis factor (TNF) antagonist therapies. ACTEMRA targets IL-6. FDA has determined that a Risk Evaluation and Mitigation Strategy (REMS) is necessary for ACTEMRA to ensure that the benefits of the drug outweigh the potential risks of serious infections, gastrointestinal perforations, changes in liver function, decreases in peripheral neutrophil counts, decreases in platelet counts, elevations in lipid parameters in peripheral blood, demyelinating disorders and malignancies.

SAFETY INFORMATION ON POTENTIAL RISKS. Serious Infections • Patients treated with ACTEMRA are at increased risk for developing serious infections leading to hospitalization or death including tuberculosis (TB), bacterial, invasive fungal, viral and other opportunistic infections. Most patients who developed these infections were taking concomitant immunosuppressants such as methotrexate or corticosteroids.• ACTEMRA should not be administered during an active infection, including localized infections. If a serious infection develops, ACTEMRA should be interrupted until the infection is controlled.• Prior to initiating ACTEMRA, a test for latent TB should be performed. If the test is positive, treatment for TB should be started prior to starting ACTEMRA. All patients should be monitored for active TB during treatment,even if the initial latent TB test is negative. Gastrointestinal Perforations• Events of gastrointestinal (GI) perforations have been reported in Phase III clinical trials, primarily as complications of diverticulitis, including generalized purulent peritonitis, lower GI perforation, fistula and abscess. ACTEMRA should be used with caution in patients who may be at increased risk for GI perforation. Patients presenting with new-onset abdominal symptoms should be evaluated promptly for early identification of GI perforation.• During the six-month Phase III clinical trials, the overall rate of GI perforations was 0.26 events per 100patient-years with ACTEMRA therapy versus no events for control.• Most patients who developed GI perforations were taking concomitant nonsteroidal anti-inflammatory medications (NSAIDs), corticosteroids or methotrexate.