Acceleration of Trichinella spiralis worm expulsion by leukotriene B4 receptor binding inhibition

Helminth infection typically induces a Th2 inflammatory response that is characterized by eosinophilia, high levels of IgE and mast cells. LTB4 is generated from innate immune cells, such as neutrophils, macrophages and mast cells, in response to a range of stimuli. It mainly acts on myeloid leukocytes, inducing the activation of integrins, adhesion to endothelium walls, and chemotaxis.

The objective of the present study was to determine the role of the LTB4 receptor in Trichinella spiralis expulsion. We treated mice with the LTB4 receptor antagonist before infection with T. spiralis. We observed that the number of mast cells and worm infection decreased following treatment with the BLT antagonist during the intestinal phase. We also demonstrated that blocking the LTB4 receptor inhibited neutrophil and eosinophil infiltration.

Further studies are required to investigate the specific mechanism of mast cell number decrease and worm infection and the in vitro interactions between LTB4 and worm expulsion.