Pharmacological strategies to resolve acute inflammation.

The inflammatory response is a physiological process that has the major role of restoring tissue homeostasis. However, uncontrolled or unresolved inflammation may cause tissue damage and contribute to the pathogenesis of chronic inflammatory and autoimmune diseases. Current pharmacological therapies to treat inflammatory maladies focus on inhibition of the productive phase of the inflammatory response including inhibition of leukocyte influx.

Treatment with a novel chemokine-binding protein or eosinophil lineage-ablation protects mice from experimental colitis.

Eosinophils are multifunctional leukocytes implicated in numerous inflammatory diseases. The present study was conducted to clarify the precise role of eosinophils in the development of colitis by using eosinophil-depleted mice and a novel chemokine-binding protein that neutralizes CCL11 action. Colitis was induced by administration of dextran sodium sulfate (DSS) to wild-type and eosinophil-deficient DeltadblGATA-1 mice.

Mechanisms underlying the inhibitory effects of tachykinin receptor antagonists on eosinophil recruitment in an allergic pleurisy model in mice.

The activation of tachykinin NK receptors by neuropeptides may induce the recruitment of eosinophils in vivo. The aim of the present study was to investigate the effects and underlying mechanism(s) of the action of tachykinin receptor antagonists on eosinophil recruitment in a model of allergic pleurisy in mice. Pretreatment of immunized mice with capsaicin partially prevented the recruitment of eosinophils after antigen challenge, suggesting the potential contribution of sensory nerves for the recruitment of eosinophils Local (10-50 nmol per pleural cavity) or systemic (100-300 nmol per animal) pretreatment with the tachykinin NK1 receptor antagonist SR140333 prevented the recruitment of eosinophils induced by antigen challenge of immunized mice.

The role of CCL22 (MDC) for the recruitment of eosinophils during allergic pleurisy in mice.

Eosinophils are important inflammatory cells in allergic diseases. In the present study, we have investigated the effects of CCL22 on the recruitment of eosinophils in vivo and in vitro. CCL22 induced a dose- and time-dependent recruitment of eosinophils into the pleural cavity of mice, and this was dependent on the release of platelet-activating factor (PAF) and subsequent generation of CCL11.