title: Chemical modulators of the innate immune response alter gypsy moth larval susceptibility to Bacillus thuringiensis.
abstract: BACKGROUND
  The gut comprises an essential barrier that protects both invertebrate and vertebrate animals from invasion by microorganisms. Disruption of the balanced relationship between indigenous gut microbiota and their host can result in gut bacteria eliciting host responses similar to those caused by invasive pathogens. For example, ingestion of Bacillus thuringiensis by larvae of some species of susceptible Lepidoptera can result in normally benign enteric bacteria exerting pathogenic effects.
  
  
  RESULTS
  We explored the potential role of the insect immune response in mortality caused by B. thuringiensis in conjunction with gut bacteria. Two lines of evidence support such a role. First, ingestion of B. thuringiensis by gypsy moth larvae led to the depletion of their hemocytes. Second, pharmacological agents that are known to modulate innate immune responses of invertebrates and vertebrates altered larval mortality induced by B. thuringiensis. Specifically, Gram-negative peptidoglycan pre-treated with lysozyme accelerated B. thuringiensis-induced killing of larvae previously made less susceptible due to treatment with antibiotics. Conversely, several inhibitors of the innate immune response (eicosanoid inhibitors and antioxidants) increased the host's survival time following ingestion of B. thuringiensis.
  
  
  CONCLUSIONS
  This study demonstrates that B. thuringiensis infection provokes changes in the cellular immune response of gypsy moth larvae. The effects of chemicals known to modulate the innate immune response of many invertebrates and vertebrates, including Lepidoptera, also indicate a role of this response in B. thuringiensis killing. Interactions among B. thuringiensis toxin, enteric bacteria, and aspects of the gypsy moth immune response may provide a novel model to decipher mechanisms of sepsis associated with bacteria of gut origin.
authors.affiliation: Department of Bacteriology, University of Wisconsin, Madison, WI 53706, USA.
authors.forename: Nichole A
authors.initials: NA
authors.lastname: Broderick
authors.forename: Kenneth F
authors.initials: KF
authors.lastname: Raffa
authors.forename: Jo
authors.initials: J
authors.lastname: Handelsman
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001413:Bacillus thuringiensis / Q000276:immunology* / Q000472:pathogenicity*; D041981:Gastrointestinal Tract / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D007113:Immunity, Innate / Q000187:drug effects*; D007155:Immunologic Factors / Q000494:pharmacology*; D007814:Larva / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D007915:Lepidoptera / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology*; D010457:Peptidoglycan / Q000494:pharmacology; D018055:Receptors, Eicosanoid / Q000037:antagonists & inhibitors; D016019:Survival Analysis
chemical_list: D000975:Antioxidants; D007155:Immunologic Factors; D010457:Peptidoglycan; D018055:Receptors, Eicosanoid