摘要 : It has been suggested that early defense mechanisms of the silkworm <i>Bombyx mori</i>, which can clear 106 bacterial cells from the hemolymph within 30 minutes, largely depend on pathogen recognition mediated by dual-carbohydrate... 展开 It has been suggested that early defense mechanisms of the silkworm <i>Bombyx mori</i>, which can clear 106 bacterial cells from the hemolymph within 30 minutes, largely depend on pathogen recognition mediated by dual-carbohydrate recognition domain (CRD) C-type lectins and nodule formation by hemocytes. In order to understand this phenomenon, the present study explores both inter- and intracellular signal transduction pathways in association with nodule formation by hemocytes of <i>B. mori</i>. The C-type lectin inhibitors dithiothreitol and ethylenediaminetetraacetic acid inhibited <i>in vivo</i> nodule formation, and a dual-CRD C-type lectin was required for <i>in vitro</i> nodule-like aggregation. These results suggested that dual-CRD C-type lectins were required as pathogen-recognition receptors for nodule formation. Serine protease inhibitors such as benzamidine hydrochloride, aprotinin, and leupeptin inhibited nodule formation, and thrombin, a serine protease, induced <i>in vivo</i> nodule-like aggregation. This indicates that serine proteases behave as mediators in the extracellular signal cascade leading to nodule formation. An inhibitor of phospholipase C, U-73122, inhibited both <i>in vivo</i> nodule formation and <i>in vitro</i> nodule-like aggregation. EDTA and pertussis toxin inhibited <i>in vivo</i> nodule formation. These results suggest that the cell reaction triggered by the two G protein-mediated signal transduction pathways plays a significant role in nodule formation. 收起