Abstract
BackgroundThe 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.ResultsWe 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.ConclusionsThis 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.
Highlights
The gut comprises an essential barrier that protects both invertebrate and vertebrate animals from invasion by microorganisms
As an initial step to distinguish between a direct or host-mediated role of gut microbiota in larval death following the ingestion of B. thuringiensis, we examined the possible association between the host immune response and larval susceptibility to B. thuringiensis
Hemocyte aggregation was observed in hemolymph samples from larvae injected with B. thuringiensis (Figure 1c), though these aggregates appeared smaller than aggregates from larvae injected with Enterobacter sp
Summary
The gut comprises an essential barrier that protects both invertebrate and vertebrate animals from invasion by microorganisms. The gut epithelium and its associated microorganisms provide an important barrier that protects animals from the external environment This barrier serves both to prevent invasion by potential pathogens and limit the elicitation of host responses to the resident microbiota [1,2]. Dysfunction of this barrier, which can occur as a result of alterations of the normal gut ecology, impairment of host immune defenses, or physical disruption of intestinal epithelia, may lead to pathological states [3,4,5,6]. The second, in which prolonged feeding on B. thuringiensis leads to developmental arrest and eventual death is thought to occur by starvation [18,19,20]
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