Chemical modulators of the innate immune response alter gypsy moth larval susceptibility to <it>Bacillus thuringiensis</it>
<p>Abstract</p> <p>Background</p> <p>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...
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doaj-4eabb4c1a1014e35b2d7d77f7771cda12020-11-24T23:18:14ZengBMCBMC Microbiology1471-21802010-04-0110112910.1186/1471-2180-10-129Chemical modulators of the innate immune response alter gypsy moth larval susceptibility to <it>Bacillus thuringiensis</it>Broderick Nichole ARaffa Kenneth FHandelsman Jo<p>Abstract</p> <p>Background</p> <p>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 <it>Bacillus thuringiensis </it>by larvae of some species of susceptible Lepidoptera can result in normally benign enteric bacteria exerting pathogenic effects.</p> <p>Results</p> <p>We explored the potential role of the insect immune response in mortality caused by <it>B. thuringiensis </it>in conjunction with gut bacteria. Two lines of evidence support such a role. First, ingestion of <it>B. thuringiensis </it>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 <it>B. thuringiensis</it>. Specifically, Gram-negative peptidoglycan pre-treated with lysozyme accelerated <it>B. thuringiensis</it>-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 <it>B. thuringiensis</it>.</p> <p>Conclusions</p> <p>This study demonstrates that <it>B. thuringiensis </it>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 <it>B. thuringiensis </it>killing. Interactions among <it>B. thuringiensis </it>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.</p> http://www.biomedcentral.com/1471-2180/10/129 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Broderick Nichole A Raffa Kenneth F Handelsman Jo |
spellingShingle |
Broderick Nichole A Raffa Kenneth F Handelsman Jo Chemical modulators of the innate immune response alter gypsy moth larval susceptibility to <it>Bacillus thuringiensis</it> BMC Microbiology |
author_facet |
Broderick Nichole A Raffa Kenneth F Handelsman Jo |
author_sort |
Broderick Nichole A |
title |
Chemical modulators of the innate immune response alter gypsy moth larval susceptibility to <it>Bacillus thuringiensis</it> |
title_short |
Chemical modulators of the innate immune response alter gypsy moth larval susceptibility to <it>Bacillus thuringiensis</it> |
title_full |
Chemical modulators of the innate immune response alter gypsy moth larval susceptibility to <it>Bacillus thuringiensis</it> |
title_fullStr |
Chemical modulators of the innate immune response alter gypsy moth larval susceptibility to <it>Bacillus thuringiensis</it> |
title_full_unstemmed |
Chemical modulators of the innate immune response alter gypsy moth larval susceptibility to <it>Bacillus thuringiensis</it> |
title_sort |
chemical modulators of the innate immune response alter gypsy moth larval susceptibility to <it>bacillus thuringiensis</it> |
publisher |
BMC |
series |
BMC Microbiology |
issn |
1471-2180 |
publishDate |
2010-04-01 |
description |
<p>Abstract</p> <p>Background</p> <p>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 <it>Bacillus thuringiensis </it>by larvae of some species of susceptible Lepidoptera can result in normally benign enteric bacteria exerting pathogenic effects.</p> <p>Results</p> <p>We explored the potential role of the insect immune response in mortality caused by <it>B. thuringiensis </it>in conjunction with gut bacteria. Two lines of evidence support such a role. First, ingestion of <it>B. thuringiensis </it>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 <it>B. thuringiensis</it>. Specifically, Gram-negative peptidoglycan pre-treated with lysozyme accelerated <it>B. thuringiensis</it>-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 <it>B. thuringiensis</it>.</p> <p>Conclusions</p> <p>This study demonstrates that <it>B. thuringiensis </it>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 <it>B. thuringiensis </it>killing. Interactions among <it>B. thuringiensis </it>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.</p> |
url |
http://www.biomedcentral.com/1471-2180/10/129 |
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