Allergic asthma is a chronic respiratory disease that affects 300 million people throughout the world. The number of people suffering from asthma has doubled over the last ten years and almost 250, 000 people die prematurely from this problem each year. In most cases, asthma is caused by an abnormal reaction to substances in the environment known as allergens. From a physiological point of view, this hypersensitivity results in serious inflammation of the bronchial tubes and the bronchioles in sensitive persons. This alters their ability to breathe correctly. Current treatment consists in administering corticoids that treat the symptoms and temporarily relieve the disorder, but without curing it. An alternative, long-lasting treatment for allergic asthma is based on a specific immunotherapeutic protocol commonly known as desensitization.
The standard test used to detect milk-protein residues in processed foods may not work as well as previously believed in all applications, sometimes missing ingredients that can cause milk allergy, the most common childhood food allergy, which affects millions of children under age 3, a scientist reported at the 243rd National Meeting & Exposition of the American Chemical Society's (ACS), the world's largest scientific society. Joseph L. Baumert, Ph.D., who headed the study, explained that thermal and non-thermal processing of foods can change the proteins responsible for milk allergy in ways that make the proteins harder to detect using the standard test, termed the enzyme-linked immunosorbent assay (ELISA). Processing, however, may still leave the milk proteins capable of causing itchy skin, runny eyes, wheezing and other sometimes more-serious symptoms of milk allergy, despite the inability to detect the milk residue.
When poet Walt Whitman wrote that we "contain multitudes, " he was speaking metaphorically, but he was correct in the literal sense. Every human being carries over 100 trillion individual bacterial cells within the intestine - ten times more cells than comprise the body itself. Now, David Artis, PhD, associate professor of Microbiology, along with postdoctoral fellow David Hill, PhD, from the Perelman School of Medicine at the University of Pennsylvania, and collaborators from The Children's Hospital of Philadelphia and institutions in Japan and Germany, have found that these commensal bacteria might play an important role in influencing and controlling allergic inflammation. The commensal relationship that develops between humans and internal bacteria is one in which both humans and bacteria derive benefits.
A new study of mice supports the idea that exposure to germs in childhood helps develop the immune system and thereby prevent allergies and other immune-related diseases such as asthma and colitis later on in life. Researchers at the Brigham and Women's Hospital in Boston, US, led the study, a report of which is in the 22 March online issue of Science. The "hygiene hypothesis" proposes that a lack of early childhood exposure to microbes increases susceptibility to certain diseases by suppressing development of the immune system. The new study not only supports this idea, but may also explain the whys and hows. However, the researchers caution that they investigated mice, and this does not necessarily mean the same results would occur in humans. The study was led by two senior authors, both from Brigham and Women's Hospital (BWH).
Previous human studies have suggested that early life exposure to microbes (i.e., germs) is an important determinant of adulthood sensitivity to allergic and autoimmune diseases such as hay fever, asthma and inflammatory bowel disease. This concept of exposing people to germs at an early age (i.e., childhood) to build immunity is known as the hygiene hypothesis. Medical professionals have suggested that the hygiene hypothesis explains the global increase of allergic and autoimmune diseases in urban settings. It has also been suggested that the hypothesis explains the changes that have occurred in society and environmental exposures, such as giving antibiotics early in life. However, neither biologic support nor a mechanistic basis for the hypothesis has been directly demonstrated. Until now.