They found that mice treated with antibiotics had elevated levels of antibodies known to be important in allergies and asthma (IgE class antibodies). The elevated antibodies in turn increased the levels of basophils, immune cells that play a role in inflammation, both allergic and otherwise.
This connection doesn’t only apply to mice but also to humans who have high levels of IgE for genetic reasons. People with genetically elevated levels of IgE are hypersusceptible to eczma and infections, and antibodies that neutralize IgE are used to treat asthma.
The antibiotic treatments and IgE did not act by promoting the survival of mature basophils, but rather by promoting the proliferation of basophil precursor cells in the bone marrow. Commensal bacteria limit this proliferative capacity.
That discovery is the real insight contributed by this paper. It has been well known for some time that IgE mediates allergies. But no one knew that bacteria living in the gut may use it to check the growth of immune precursor cells in the bone marrow. The finding might have wide ranging implications and help us make sense of other chronic inflammatory disease states that have also been associated with changes in this bacterial populations. Commensal bacteria might impact these other inflammatory conditions—including cancer, infection, and autoimmune disorders—through this mechanism, as well.
Experts have puzzled over the enormous explosion of asthma and allergies in recent years, and been unable to pinpoint the cause. This paper suggests that perhaps the overuse of antibacterial products could be to blame.
Nature Medicine, 2012. DOI: 10.1038/nm.2657 (About DOIs).