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Research suggests beta agonists may alter the immune system
November 17, 2006WINSTON-SALEM, N.C. - New research at Wake Forest University School of Medicine suggests that certain inhaled asthma medications - as well as similar chemicals our bodies produce during times of high stress - may worsen diseases such as asthma, heart failure and lupus that involve inflammation.
The scientific team led by Raymond Penn, Ph.D., and Matthew Loza, Ph.D, found that beta-agonists, such as those used in the treatment of asthma, increase the accumulation of type 2 T cells, a type of white blood cell that participates in immune system defense mechanisms. In certain diseases such as asthma and lupus, an over-reactive type 2 T cell response occurs and is believed to contribute to the disease.
"Inhaled beta-agonists are very effective in opening up airways and allowing asthmatics to breathe, but their ability to address the underlying inflammation that causes most asthma has been debated for years," said Penn, an associate professor in the Department of Internal Medicine and the Center for Human Genomics.
The research is reported on-line in the Journal of Allergy and Clinical Immunology and will be published in an upcoming print issue.
In fact, numerous clinical studies have reported that asthma symptoms tend to worsen over time in patients on continuous beta-agonist therapy. Although the reasons for this deterioration of asthma control are not clear, the Food and Drug Administration now recommends that the treatment of asthma with long-acting beta-agonists be supplemented with inhaled anti-inflammatory medications.
Using blood samples from human participants, the scientists measured the effect of beta-agonists on white blood cells that were grown in the laboratory. They were surprised to find that the drugs promoted a preferential accumulation of type 2 T cells.
Beta-agonists belong to a class of chemicals that include the hormone adrenaline produced by the body. Consequently, conditions that elevate blood adrenaline, such as emotional stress or heart failure, may also have the ability to alter the immune system by increasing type 2 T cells, and thereby promote or worsen disease.
"Although further research is needed to confirm that these findings occur in the human body, our research points to an important means by which the immune system is regulated by both therapies and the hormonal system," Penn said. "From an asthma management standpoint, these studies further emphasize the need to include anti-inflammatory corticosteroids when treating moderate to severe asthma."
The researchers also uncovered the mechanism which by beta-agonists increased type 2 T cells. They found that the beta-agonists were unable to effectively stimulate the enzyme protein kinase A (PKA). Other molecules similar to beta-agonists that were able to strongly activate PKA also inhibited the ability of type 2 T cells to proliferate and survive. Penn said this finding could influence future drug development, because new beta agonists that are more effective in activating PKA may prove useful.
Wake Forest University Baptist Medical Center
The research is reported on-line in the Journal of Allergy and Clinical Immunology and will be published in an upcoming print issue.
In fact, numerous clinical studies have reported that asthma symptoms tend to worsen over time in patients on continuous beta-agonist therapy. Although the reasons for this deterioration of asthma control are not clear, the Food and Drug Administration now recommends that the treatment of asthma with long-acting beta-agonists be supplemented with inhaled anti-inflammatory medications.
Using blood samples from human participants, the scientists measured the effect of beta-agonists on white blood cells that were grown in the laboratory. They were surprised to find that the drugs promoted a preferential accumulation of type 2 T cells.
Beta-agonists belong to a class of chemicals that include the hormone adrenaline produced by the body. Consequently, conditions that elevate blood adrenaline, such as emotional stress or heart failure, may also have the ability to alter the immune system by increasing type 2 T cells, and thereby promote or worsen disease.
"Although further research is needed to confirm that these findings occur in the human body, our research points to an important means by which the immune system is regulated by both therapies and the hormonal system," Penn said. "From an asthma management standpoint, these studies further emphasize the need to include anti-inflammatory corticosteroids when treating moderate to severe asthma."
The researchers also uncovered the mechanism which by beta-agonists increased type 2 T cells. They found that the beta-agonists were unable to effectively stimulate the enzyme protein kinase A (PKA). Other molecules similar to beta-agonists that were able to strongly activate PKA also inhibited the ability of type 2 T cells to proliferate and survive. Penn said this finding could influence future drug development, because new beta agonists that are more effective in activating PKA may prove useful.
Wake Forest University Baptist Medical Center
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Factors from common human bacteria may trigger multiple sclerosis
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Surface bacteria maintain skin's healthy balance
On the skin's surface, bacteria are abundant, diverse and constant, but inflammation is undesirable. Research at the University of California, San Diego School of Medicine now shows that the normal bacteria living on the skin surface trigger a pathway that prevents excessive inflammation after injury.
Gene mismatch influences success of bone marrow transplants
A commonly inherited gene deletion can increase the likelihood of immune complications following bone marrow transplantation, an international team of researchers reports in the November 22 advance online issue of Nature Genetics.
Measuring and modeling blood flow in malaria
When people have malaria, they are infected with Plasmodium parasites, which enter the body from the saliva of a mosquito, infect cells in the liver, and then spread to red blood cells.
New cancer target for non-Hodgkin's lymphoma
Physician-scientists from Weill Cornell Medical College have discovered a molecular mechanism that may prove to be a powerful target for the treatment of non-Hodgkin's lymphoma, a type of cancer that affects lymphocytes, or white blood cells.
First reconstitution of an epidermis from human embryonic stem cells
Stem cell research is making great strides. This is yet again illustrated by a study carried out by the I-STEM* Institute (I-STEM/ Inserm UEVE U861/AFM), published in the Lancet on 21 November 2009. The I-STEM team, directed by Marc Peschanski has just succeeded in recreating a whole epidermis from human embryonic stem cells.
New findings suggest strategy to help generate HIV-neutralizing antibodies
New discoveries about anti-HIV antibodies may bring researchers a step closer to creating an effective HIV vaccine, according to a new paper co-authored by scientists at the Vaccine Research Center of the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.
UAB Researchers Discover Antibody Receptor Identity, Propose Renaming Immune-System Gene
Researchers at the University of Alabama at Birmingham (UAB) have uncovered the genetic identity of a cellular receptor for the immune system's first-response antibody, a discovery that sheds new light on infection control and immune disorders.
New culprit for viral infections among elderly -- an overactive immune response
Researchers at Yale School of Medicine have found that exaggerated responses of the immune system explain why the elderly succumb to viral infections more readily than younger people.
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