Insect immune response to bacterial infection is mediated by eicosanoids

David W. Stanley-Samuelson, Ellen Jensen, Kenneth W. Nickerson, Kristina Tiebel, Clyde L. Ogg, Ralph W. Howard

Research output: Contribution to journalArticle

147 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1064-1068
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume88
Issue number3
DOIs
StatePublished - 1991

Keywords

  • Cyclooxygenase
  • Lipoxygenase
  • Manduca sexta
  • Phospholipase A
  • Serratia marcescens

ASJC Scopus subject areas

  • General

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