So then why do food allergies impact some 5 percent of all U.S. children when food is not directly harmful? The reasons still remain poorly understood, and these studies do not address them. Foods may have proteins that remind the body of other, harmful substances or are related to toxic plants. Thus, in the course of evolution our bodies may have unwittingly lumped them into the same category, Medzhitov says.
As for why allergies are seemingly on the rise, this work does nothing to dispel or support the so-called hygiene hypothesis, which links allergies to modern hyperclean environments. With the advent of clean water and childhoods devoid of consuming much dirt (and the millions of bacteria and viruses that come with them) the immune system does not receive the early training it needs to function correctly, the hypothesis says. A healthy exposure to those invaders leads the body to invest more in type 1 responses, including strong microbe defense, rather than type 2 reactions such as allergies.
The Stanford team simulated both bee stings and snakebites in two separate strains of mice to examine the extent to which genetics influences the immune response. They found that prior exposure to the venoms provided significant protections in both strains. When the mice were exposed to the bee venom and then reexposed three weeks later at least 80 percent survived; of the mice that were not similarly inoculated, under 30 percent managed to survive. Simulated snakebites among mice led to a similar death toll, with at least three quarters of venom-exposed mice surviving compared with only about a quarter of the control group. Moreover, in the case of honeybee venom this protection was transferable; unexposed mice injected with serum containing circulating bee-venom specific antibodies from the venom-injected mice experienced some protection when they encountered a near-lethal dose of venom 20 hours later.
The Yale team testing bee and snake venom exposures also found that after six weekly immunizations of an enzyme common across multiple venoms, mice reexposed to the enzyme after a week off were afforded better protection than their unimmunized brethren. In nature each venom may have slightly different impacts on the body in their whole form, but by focusing on this enzyme the investigators could study the molecular pathway that might trigger the body’s development of antibodies to multiple venoms, potentially setting the stage for future therapies, the authors say. Not all venoms contain this particular enzyme, but the findings, coupled with Stanford’s, provide new insights into allergen interactions with the body.
“It’s really hard to say if this will change the way people with allergies are treated or manage it, but at least physicians can say it’s not a total mystery why these allergies developed,” Galli remarks. The point of these works was to figure out why allergies exist at all, so we are still far from providing therapies based on these findings, Medzhitov says. The line between protection and anaphylaxis with venom is still narrow and we still don’t know what controls the transition from protective response to a deadly one, preventing any immediate treatments for now.