To some people, allergies are an annoyance that they have to deal with every spring. To others, allergies are a life-threatening illness that could strike if they eat the wrong food. Regardless of their severity, the prevalence of allergies as a whole has increased rapidly around the globe.
As the world becomes more globalized, there is a clear increase in the number of people affected by them. A study conducted by the Centers for Disease Control in May 2013 stated that there was an 18 percent increase in food allergies between 1997 and 2007. Also, the rate rose significantly in families with an income 200 percent or more above the poverty level.
There is no question that there have been vast lifestyle changes over the last few centuries. There are also large differences in the quality of life from an undeveloped country to a developed one. Babies are born by Cesarean section and fed formula, we live near-sterilized lifestyles, prescription of antibiotics has increased... the list goes on.
The correlation between this change in lifestyle and an increase in allergies seems to support the “hygiene hypothesis” first stated in the British Medical Journal in 1989. The hypothesis was developed when researchers looked at the relationship between hay fever and exposure to infectious agents, and it is now being thoroughly considered by immunologists and epidemiologists alike. The “hygiene hypothesis” states that humans’ efforts to decrease their exposure to different microbes and infectious agents has led to an immune system that is less capable of fighting off simple allergenic compounds.
Although less was known about microbiology at the time this theory was proposed, it is an area of quickly growing research. With the NIH’s Human Microbiome Project, begun in 2007, and other side projects such as the American Gut Project, it looks like we will see a lot more research into the human microbiome and its association with various medical conditions.
A study published Aug. 25 in Proceedings of the National Academy of Sciences has connected the growth of a specific species of bacteria to decreased allergen sensitization in mice. In a sea of trillions of bacteria, the human gastrointestinal tract must be capable of deciding when to remain unresponsive to antigens and when to trigger the responses of Immunoglobulin A, or IgA, which is responsible for mucosal immunity, and regulatory T cells, which differentiate between the body’s own antigens and antigens from outside.
Researchers at the University of Chicago used a mouse model to study this phenomenon. Two very controlled types of mice were used: germ-free mice, and “typical specific pathogen-free” mice, which contained normal microbial agents.
Upon treatment with peanut allergens, the germ-free mice displayed a clear difference in cecal size and higher levels of Immunoglobulin E, or IgE. The cecum is a pouch in the beginning of the large intestine measured to indicate potential inflammation in the GI tract. IgE is responsible for immunity to parasites and was measured to compare the organism’s response to antigens.
Two species of bacteria that are prevalent in a normal mouse intestinal microbiota were then considered for the next trials: Bacteroids uniformis and Clostridium clusters XIVa, XIVb and IV. Of the two, only Clostridia was found capable of protecting mice from the peanut allergens: It reduced the cecal size and the amount of IgA produced.
The next step was surveying the effects of antibiotics on neonatal mice, and trying to restore the intestinal microbial community. After antibiotic administration, the mice’s microbiomes were allowed to recover from antibiotics or restored with either conventional microbiota or Clostridia. These three mouse strains responded similarly, with a reduced immunoglobulin antibody response. Scientists concluded that Clostridia was enough to restore and protect against food allergens.
The last part of the study covered the mechanism through which Clostridia was aiding the organism. With the use of microarray technology, this species was found to produce IL-22, which reduced the permeability of distinct food antigens into the bloodstream. Regulatory T cells and IgA levels were also assessed. Mice with Clostridia-containing microbiota displayed an expansion of regulatory T cells that augmented the environment’s ability to maintain antigen tolerance. There was also a class switch from IgE to IgA, leading to the conclusion that IgA helped diminish the allergen intake as well.
Although this study was conducted in mice, it poses an interesting possibility. With this advancement in place, there is hope for an improved probiotic treatment in humans that might rid 15 million Americans from the burden of allergies.
