99th Dahlem conference on infection, inflammation and chronic inflammatory disorders: the role of infections in allergy: atopic asthma as a paradigm

Abstract

Earlier iterations of the 'hygiene hypothesis', in which infections during childhood protect against allergic disease by stimulation of the T helper type 2 (Th2)-antagonistic Th1 immunity, have been supplanted progressively by a broader understanding of the complexities of the underlying cellular and molecular interactions. Most notably, it is now clear that whole certain types of microbial exposure, in particular from normal gastrointestinal flora, may provide key signals driving postnatal development of immune competence, including mechanisms responsible for natural resistance to allergic sensitization. Other types of infections can exert converse effects and promote allergic disease. We review below recent findings relating to both sides of this complex picture.

Fig. 1

Risk for virus infections that spread from the upper to the lower respiratory tract, and for sensitization to aeroallergens, is maximal in the first few years of life, due mainly to maturational deficiencies in innate and adaptive immune functions during this life phase. Microbial exposure (particularly via the gut) can, on one hand, protect against both processes via promoting functional maturation of immune competence, but in other circumstances (exemplified by severe respiratory viral infections) can interact synergistically with underlying atopic inflammation to promote development of clinically relevant allergic disease.