Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/54296
Title: Cytoplasmic signalling pathways in alveolar macrophages involved in the production of nitric oxide after stimulation with excretory/secretory antigens of Toxocara canis
Authors: Espinoza, Elsa
Pérez-Arellano, José Luis 
Vicente, Belén
Muro, Antonio
Keywords: Protein-Kinase-C
Nf-Kappa-B
Phospholipase A(2)
Lung Injury
Calcium, et al
Issue Date: 2002
Publisher: 0141-9838
Journal: Parasite Immunology 
Abstract: We studied the cytoplasmic signalling pathways involved in the generation of nitric oxide (NO) after stimulation with adult e x cretory/secretory antigens (ESA) of Toxocara canis. The pathways of phospholipase A2 (PLA2) and phospholipase C (PLC) were considered as potentially involved in the synthesis of nitric oxide. We used inhibitors of these pathways at different levels. Several concentrations of lithium chloride, verapamil, TMB-8 and staurosporine were used to inhibit the PLC pathway. Inhibition of the PLA2 pathway was attempted with mepacrine, diethylcarbamazine or meloxicam. Lithium chloride, verapamil and TMB-8 reduced the production of NO induced by ESA in a concentration-dependent manner. Regarding the PLA2 pathway, a range of concentrations of mepacrine greatly reduced the production of NO induced by ESA. Meloxicam inhibition was always higher than 50%. Diethylcarbamazine showed a dose-dependent effect on the production of NO induced by the ESA. Our results suggest that both the PLC and the PLA2 pathways play an essential role in activating the production of macrophage NO triggered by the ESA of T. canis. This could indicate that NO production in our experimental conditions is due to both an increase of intracellular calcium and to the participation of the arachidonic acid cascade. The implications of these activations on the host-parasite relationship are discussed and compared with LPS-stimulated macrophages.
URI: http://hdl.handle.net/10553/54296
ISSN: 0141-9838
DOI: 10.1046/j.1365-3024.2002.00597.x
Source: Parasite Immunology[ISSN 0141-9838],v. 24, p. 535-544
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