Targeting allergic airway diseases by siRNA: an option for the future?

Allergic diseases emerge as a substantial health problem of the 21(st) century. Current therapies including combination therapies of corticosteroids and beta(2)-agonists are highly effective, inexpensive and relatively safe. However, these medicaments only relieve symptoms but are not curing disease.

Cis-9,trans-11-conjugated linoleic acid inhibits allergic sensitization and airway inflammation via a PPARgamma-related mechanism in mice.

Milk consumption from early childhood on has been found to be inversely correlated with allergic sensitization and the onset of bronchial asthma. We tested whether cis-9,trans-11-conjugated linoleic acid (c9,t11-CLA), naturally occurring in milk fat, may prevent allergic sensitization and inhibit airway inflammation in a murine asthma model. BALB/c mice were fed a diet enriched in 1 wt% of c9,t11-CLA or a control diet 7 d prior to and for 32 d during sensitization [d 1 and 14, 100 mg/L ovalbumin (OVA) in adjuvant vs.

Primary prevention of allergic diseases: current concepts and mechanisms.

: Atopic diseases, the new "epidemic of the twenty-first century" and a central health problem of industrial nations, call for the development of innovative primary prevention strategies. The present review provides an overview of current experimental and immunomodulatory procedures and their underlying mechanisms.

Immunoprophylaxis with DNA vaccination inhibits Th2-mediated responses and airway inflammation in mice sensitised with the major timothy grass pollen allergen Phl p 5b.

DNA vaccination is discussed as having the potential of improving therapy of type I allergies. A mouse model was used to investigate the effect of DNA vaccination against sensitisation with the clinically relevant Phl p 5b major allergen from timothy grass pollen in an immunoprophylactic experimental setup. Pre-treating the mice with Phl p 5b-DNA-construct significantly inhibited the production of specific IgE and IgG1 antibodies and prevented the development of a lung pathology associated with inflammation.