Surface antigens of Xenorhabdus nematophila (F. Enterobacteriaceae) and Bacillus subtilis (F. Bacillaceae) react with antibacterial factors of Malacosoma disstria (C. Insecta: O. Lepidoptera) hemolymph.
Previous research established different interactions of the insect pathogen, Xenorhabdus nematophila and nonpathogen, Bacillus subtilis, with antimicrobial hemocytes and humoral factors of larval Malacosoma disstria [Giannoulis, P., Brooks, C.L., Dunphy, G.B., Mandato, C.A., Niven, D.F., Zakarian, R.J., 2007. Interaction of the bacteria Xenorhabdus nematophila (Enterobacteriaceae) and Bacillus subtilis (Bacillaceae) with the hemocytes of larval Malacosoma disstria (Insecta: Lepidoptera: Lasicocampidae). J. Invertebr. Pathol. 94, 20-30]. The antimicrobial systems were inhibited by X. nematophila and stimulated by B. subtilis. The bacterial surface antigens participating in these reactions were unknown. Thus, herein the effects of lipopolysaccharide (endotoxin) from X. nematophila and lipoteichoic acid from B. subtilis on the larval M. disstria immune factors, the hemocytes and phenoloxidase, were determined. Endotoxin elevated the level of damaged hemocytes limiting the removal of X. nematophila from the hemolymph and enhancing the rapid release of bacteria trapped by nodulation. Similar effects were observed with the lipid A moiety of the endotoxin. The effects of lipopolysaccharide and lipid A on the hemocyte activities were abrogated by polymyxin B (an antibiotic that binds to lipid A) confirming lipopolysaccharide as the hemocytotoxin by virtue of the lipid A moiety. Lipoteichoic acid elicited nodulation and enhanced phenoloxidase activation and/or activity. Although lipoidal endotoxin and lipid A inhibited phenoloxidase activation they enhanced the activity of the enzyme. Apolipophorin-III precluded the effects of lipopolysaccharide, lipid A, and lipoteichoic acid on the hemocytes and prophenoloxidase until the antigens exceeded a critical threshold.
Giannoulis
Paschalis
P
Department of Natural Resource Sciences, Macdonald Campus of McGill University, 21, 111 Lakeshore Road, Ste. Anne de Bellevue, Que., Canada H9X 3V9.
Brooks
Cory L
CL
Dunphy
Gary B
GB
Niven
Donald F
DF
Mandato
Craig A
CA
D000818:Animals; D000954:Antigens, Surface / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology; D001053:Apolipoproteins / Q000276:immunology / Q000494:pharmacology; D001412:Bacillus subtilis / Q000276:immunology / Q000378:metabolism*; D002452:Cell Count; D004306:Dose-Response Relationship, Immunologic; D006434:Hemocytes / Q000187:drug effects / Q000382:microbiology; D054884:Host-Pathogen Interactions; D066298:In Vitro Techniques; D007814:Larva / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D008050:Lipid A / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology*; D014442:Monophenol Monooxygenase / Q000276:immunology; D009036:Moths / Q000187:drug effects* / Q000276:immunology* / Q000382:microbiology; D013682:Teichoic Acids / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology*; D020593:Xenorhabdus / Q000276:immunology / Q000378:metabolism*
D000954:Antigens, Surface; D001053:Apolipoproteins; D008050:Lipid A; D008070:Lipopolysaccharides; D013682:Teichoic Acids; C042470:apolipophorin III; C009900:lipoteichoic acid; D014442:Monophenol Monooxygenase