The cytosolic nucleotide oligomerization domain (NOD)-like receptors NOD1 and 
NOD2 are important contributors to the intracellular recognition of pathogens 
including Chlamydophila pneumoniae, but little is known about their influence on 
allergen-induced airway inflammation. In BALB/c mice, we observed that infection 
with C. pneumoniae before systemic sensitization with ovalbumin (OVA) and local 
OVA airway exposure diminished airway hyperresponsiveness (AHR). Thus, the 
impact of the NOD1 agonist FK156 and the NOD2 agonist muramyl dipeptide given 6 
hours before each sensitization or airway challenge was evaluated regarding AHR, 
OVA-specific plasma immunoglobulins, bronchoalveolar lavage fluid differentials, 
and cytokines. Spleen dendritic cells of FK156-treated mice were isolated and 
cocultured with OVA-specific T cells isolated from DO11.10 mice, and T-cell 
proliferation was quantified after OVA restimulation. T-cell proliferation was 
investigated in vivo in lungs and lymph nodes of FK156-treated and OVA-exposed 
DO11.10 mice. FK156, but not muramyl dipeptide, reduced AHR and pulmonary 
eosinophilic infiltration if given before OVA sensitization or challenge, 
whereas T-helper (Th)2 cytokines were not diminished. Dendritic cells from 
FK156-treated mice evoked less OVA-specific T-cell proliferation as compared 
with solvent-treated controls. Similarly, antigen-specific T-cell activation in 
lung tissue was diminished after FK156 treatment. We conclude that NOD1 
activation reduced AHR in allergen-induced lung inflammation, which was 
accompanied by a reduction of allergen-specific T-cell proliferation.