Abstract
The incidence and severity of allergic asthma have increased over the last century, particularly in the United States and other developed countries. This time frame was characterized by marked environmental changes, including enhanced hygiene, decreased pathogen exposure, increased exposure to inhaled pollutants, and changes in diet. Although iron is well-known to participate in critical biologic processes such as oxygen transport, energy generation, and host defense, iron deficiency remains common in the United States and world-wide. The purpose of these studies was to determine how dietary iron supplementation affected the severity of allergic inflammation in the lungs, using a classic model of IgE-mediated allergy in mice. Results showed that mice fed an iron-supplemented diet had markedly decreased allergen-induced airway hyperreactivity, eosinophil infiltration, and production of pro-inflammatory cytokines, compared with control mice on an unsupplemented diet that generated mild iron deficiency but not anemia. In vitro, iron supplementation decreased mast cell granule content, IgE-triggered degranulation, and production of pro-inflammatory cytokines post-degranulation. Taken together, these studies show that iron supplementation can decrease the severity of allergic inflammation in the lung, potentially via multiple mechanisms that affect mast cell activity. Further studies are indicated to determine the potential of iron supplementation to modulate the clinical severity of allergic diseases in humans.
Highlights
Under normal conditions, the immune system responds to common ingested or inhaled antigens by inducing a state of specific non-responsiveness called tolerance
We recently identified iron deficiency as a trigger for increased mast cell activation that was associated with mast cell-dependent hair loss in IL-10-deficient (Il102/2) mouse pups [5]
The eosinophils present in bronchoalveolar spaces decreased from 192,679612,608 eosinophils/ml Bronchoalveolar lavage (BAL) fluid in OVA-challenged unsupplemented mice (95% of total cells; n = 5 mice) to 93,224613,770 eosinophils/ ml in OVA-challenged iron-supplemented mice (85% of total cells; n = 5 mice), a decrease of,50%
Summary
The immune system responds to common ingested or inhaled antigens by inducing a state of specific non-responsiveness called tolerance. Mast cell degranulation induces a cascade that results in infiltration by immune cells and and stimulates de novo production of additional inflammatory mediators. Asthma is a chronic inflammatory disease of the airways associated with airway hyperresponsiveness that often occurs in allergic patients. Current treatments that decrease the severity of airway obstruction include bronchodilators and corticosteroids, but these fail to address any underlying allergic reactions. Methods to decrease the severity of allergic reactions include IgE depletion using anti-IgE monoclonal antibodies, induction of IgG blocking antibodies by allergen immunotherapy, and blocking downstream effects of mast cell degranulation using antihistamines or corticosteroids. Identification of additional therapies that could prevent or decrease the severity of allergic reactions would provide a major improvement in clinical care of patients with allergen-triggered asthma
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
