Insect immune response to bacterial infection is mediated by eicosanoids

Authors

David W. Stanley-Samuelson, University of Nebraska-Lincoln
Ellen Jensen, University of Nebraska-LincolnFollow
Kenneth Nickerson, University of Nebraska-LincolnFollow
Kristina C. Tiebel, University of Nebraska-LincolnFollow
Clyde Ogg, University of Nebraska-LincolnFollow
Ralph W. Howard, United States Department of Agriculture/Agricultural Research Service U.S. Grain Marketing Research Laboratory

Document Type

Article

Date of this Version

2-1-1991

Comments

Published in Proc. Nati. Acad. Sci. USA Vol. 88, pp. 1064-1068, February 1991.

Abstract

Inhibition of eicosanoid formation in larvae of the tobacco hornworm Manduca sexta, using specific inhibitors of phospholipase A₂, cyclooxygenase, and lipoxygenase, severely weakened the ability of larvae to clear the bacterium Serratia marcescens from their hemolymph. The reduced capability to remove bacteria is associated with increased mortality due to these bacteria. There is a dose-dependent relationship between the phospholipase A₂ inhibitor dexamethasone and both the reduced bacterial clearance and increased larval mortality. The dexamethasone effects on larval survival were reversed by treatment with arachidonic acid. Maleic acid, a nonspecific antioxidant, did not interfere with the insects' ability to remove bacterial cells from hemolymph. The larvae were shown to contain all of the C₂₀ polyunsaturated fatty acids necessary for eicosanoid biosynthesis and to be capable of converting radioactive arachidonic acid into several primary prostaglandins. These results strongly suggest that eicosanoids mediate transduction of bacterial infection signals into the complex of cellular and humoral responses that comprise invertebrate immunity.