Insect immune response to bacterial infection is mediated by eicosanoids.

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 marscescens 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.

authors

Stanley-Samuelson DW,Jensen E,Nickerson KW,Tiebel K,Ogg CL,Howard RW

doi

10.1073/pnas.88.3.1064

subject

Has Abstract

pub_date

1991-02-01 00:00:00

pages

1064-8

issue

3

eissn

0027-8424

issn

1091-6490

journal_volume

88

pub_type

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