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Title: EICOSANOIDS MEDIATE MANDUCA SEXTA CELLULAR RESPONSE TO BEAUVERIA BASSIANA: A ROLE FOR THE LIPOXYGENASE PATHWAY

Author
item Lord, Jeffrey
item Anderson, Sheri
item STANLEY, DAVID - UNIV NEBRASKA

Submitted to: Archives of Biochemistry and Biophysics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/30/2002
Publication Date: 9/5/2002
Citation: Lord, J.C., Anderson, S.A., Stanley, D.W. 2002. Eicosanoids mediate manduca sexta cellular response to beauveria bassiana: a role for the lipoxygenase pathway. Archives Of Biochemistry And Physiology 51: 46-54.

Interpretive Summary: Microbes that attack insects are safe alternatives to chemical insecticides, but concerns about the speed of action and consistency has limited their use. Insects respond to challenge from disease-causing microbes by engulfing them in individual blood cells and by encasing them in nodules formed by assemblages of blood cells and by activated pigment-producing enzymes. Signaling compounds, called eicosanoids, have been implicated in the initiation of these processes in response to bacteria. We have used drugs that inhibit the synthesis of these signal compounds to demonstrate that they are also needed for the response to a fungus that is pathogenic for insects. We have also used specific inhibitors and synthesis intermediates to determine the type of eicosanoid that is needed for the nodulation process. This information will help us to find ways to defeat insect defenses against disease organisms and improve the performance of microbial insecticides.

Technical Abstract: Many studies have documented the involvement of eicosanoids in insect cellular immune responses to bacteria. The use of Beauveria bassiana as a nodulation elicitor, with inhibition of phospholipase A2 by dexamethasone extends the principal to fungi. This study also provides the first evidence of involvement of the lipoxygenase (LOX) pathway rather than the cyclooxygenase (COX) pathway in synthesis of the nodulation mediating eicosanoid(s). The LOX product, 5(S)-hydroperoxyeicosa-6E,8Z,11Z,14Z-tetraenoic acid (5-HPETE), substantially reversed nodulation inhibition by dexamethasone and the LOX inhibitors, caffeic acid and esculetin. The COX product, prostaglandin H2 (PGH2), did not reverse the nodulation inhibition by dexamethasone or the COX inhibitor, ibuprofen. None of the inhibitors tested had a significant effect on phagocytosis of B. bassiana blastospores in vitro. Hemocyte phenoloxidase activity was reduced by dexamethasone, esculetin, and the COX inhibitor, indomethacin. The rescue candidates 5-HPETE and PGH2, rather than reversing the inhibition, depressed phenoloxidase activity further.