While our primary concern is the impact that the innate immune system has on allergic disease, it is essential to recognize that allergic disease also impacts on the function- ing of the innate immune system. In part this is through treatment, since immunosuppressive therapies inevitably contribute to impairment of immunity at the levels of the innate and adaptive systems.
Induction of inflammation might be thought to generate a local environment that is hostile to pathogens, and allergen provocation of the nose can, for example, enhance subsequent responses to endotoxin. Beyond this, asthma itself is a risk factor for invasive pneumococcal disease. Macrophages are crucial in defense against pneumococccus. It is interesting to note, therefore, that the phenotype of allergic disease and the response to infection may rest in part in macrophage phenotypes that may be better or worse at supporting Th2 and Th1 responses. Susceptibility to pneumococcal disease in different mouse strains is potentially associated with their ability to recruit and activate neutrophils.
Allergic inflammation further degrades the function of innate immunity, through suppression of the generation of antimicrobial peptides such as defensins from the epithelium, resulting in increased susceptibility to Pseudomonas aeruginosa infections in mouse models. Abnormalities in the bronchial epithelium also appear to underlie risk factors for viral infection, since asthmatic airway epithelium shows an impaired interferon response to viral infection. It is interesting to note that local immunity may be impaired even in the presence of a potentially vigorous chronic inflammatory response. Indeed, chronic inflammation may for other reasons provide an environment with potentially advantageous components from the point of view of the respiratory pathogen.
Barrier disruption by epithelial damage may favor pathogen access, and up regulation of tissue cell adhesion molecule expression may make viral attachment and infection easier.
