Abstract
Deficient microbial stimulation of the immune system, caused by hygiene, may underly the atopy and allergic asthma epidemic we are currently experiencing. Consistent with this 'hygiene hypothesis', research on immunotherapy of allergic diseases also centres on bacteria-derived molecules (eg DNA immunostimulatory sequences) as adjuvants for allergen-specific type 1 immune responses. If we understood how certain microbes physiologically 'educate' our immune system to interact safely with environmental nonmicrobial antigens, we might be able to learn to mimic their beneficial actions. Programmed 'immunoeducation' would consist of safe administration, by the correct route, dose and timing, of those microbial stimuli that are necessary to 'train' the developing mucosal immune system and to maintain an appropriate homeostatic equilibrium between its components. Overall, this would result in a prevention of atopy that is not limited to certain specific allergens. Although such a strategy is far beyond our present potential, it may in principle revert the epidemic trend of atopy and allergic asthma without jeopardizing the fight against infectious diseases.
Highlights
Allergic asthma is on the increase in Western countries, as are efforts to identify the reasons for this increase [1]
The hygiene hypothesis has been suggested. According to this hypothesis, changing interactions between humans and microbes of their ecosystem alter the immune balance at mucosal level between type 1 (Th1, Tcl) and type 2 (Th2, Tc2) immunity, thereby predisposing to atopic diseases [5,6], including allergic asthma
Less indirect support for the hygiene hypothesis came from epidemiological studies of Italian military cadets [19,20], which showed that exposure to food-borne and orofaecal infections, but not to air-borne viruses, was inversely associated with respiratory allergies
Summary
Allergic asthma is on the increase in Western countries, as are efforts to identify the reasons for this increase [1]. Less indirect support for the hygiene hypothesis came from epidemiological studies of Italian military cadets [19,20], which showed that exposure to food-borne and orofaecal infections, but not to air-borne viruses, was inversely associated with respiratory allergies These serological studies support the notion that a high turnover of ingested microbes (mainly saprophytic, commensal and pathogen bacteria) at mucosal surfaces, in particular the gut mucosa, may ‘educate’ our mucosal immune system to interact safely with nonmicrobial antigens [21,22,23,24]. The concentration of exogenous lipopolysaccharide in house dust was inversely related to atopy among infants at risk for asthma [26] This suggests that ingested bacteria, and bacterial immunostimulating substances from inhalable sources could afford protection against allergy. This approach may be helpful in preventing atopy with a more ‘physiological’ stimulation, without the need of immunizing against all of the allergens that are potentially encountered during a whole lifetime
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