We showed that ongoing allergic rhinitis augments the response to an acute bacterial infection (Blair JACI 108:424–429, 2001). To test whether histamine was responsible for this increase, we studied the effect of an H1 receptor antagonist, desloratadine.

Three groups of mice were studied: 1) infected mice, 2) infected and allergic mice treated with desloratadine, and 3) infected and allergic mice treated with placebo. BALB/c mice were sensitized to ovalbumin by 2 intraperitoneal injections. Next, they were challenged daily with 6% OVA for 5 days. After the second OVA challenge, all mice were intranasally inoculated with S. pneumoniae. Desloratadine or placebo was given daily throughout the exposure period. Nasal allergic symptoms were observed after each exposure. On day 5 post-infection, nasal lavages were quantitated for S. pneumoniae and the inflammatory cells in the sinuses were evaluated.

Mice that were made allergic, infected and treated with placebo, showed more organisms and phagocytic cells than just infected, nonallergic mice. They also manifested increased allergic symptoms and number of eosinophil influx into the sinuses. Compared to the placebo treated group, desloratadine treatment during allergen exposure inhibited allergic symptoms and reduced the recovery of S. pneumoniae in nasal lavages (p<0.05 both). The desloratadine treated group also tended to have less neutrophil influx (p=0.09 both), but no change in eosinophil influx (p=0.85) compared to placebo treated group.

Desloratadine treatment inhibited allergic symptoms and reduced sinonasal infection, suggesting that histamine plays a role in the augmented response to infection in mice with an ongoing allergic reaction.