TY - JOUR
T1 - Modulation of social interactions by immune stimulation in honey bee, Apis mellifera, workers
AU - Richard, Freddie Jeanne
AU - Aubert, Arnaud
AU - Grozinger, Christina M.
N1 - Funding Information:
We would like to thank Coby Schal and Michael Roe for use of their GC and GC/MS instruments, Lillian King for her assistance in the behavioral test observations of individual bees, and Joe Flowers for expert beekeeping assistance. We would also like to thank Kevin Donohue, Toshi Nojima, Dorit Eliyahu, Elsa Youngsteadt for their assistance in the GC set up and Coby Schal for interesting discussions. We would also like to thank Gene Robinson for reading an earlier version of the manuscript. This work was partially supported by funding from a USDA-NRI grant to CMG and FJR (2007-02284). FJR was supported by post-doctoral fellowships from the Conseil Regional d'Indre et Loire, France and the North Carolina State University WM Keck Center for Behavioral Biology.
PY - 2008/11/17
Y1 - 2008/11/17
N2 - Background: Immune response pathways have been relatively well-conserved across animal species, with similar systems in both mammals and invertebrates. Interestingly, honey bees have substantially reduced numbers of genes associated with immune function compared with solitary insect species. However, social species such as honey bees provide an excellent environment for pathogen or parasite transmission with controlled environmental conditions in the hive, high population densities, and frequent interactions. This suggests that honey bees may have developed complementary mechanisms, such as behavioral modifications, to deal with disease. Results: Here, we demonstrate that activation of the immune system in honey bees (using bacterial lipopolysaccharides as a non-replicative pathogen) alters the social responses of healthy nestmates toward the treated individuals. Furthermore, treated individuals expressed significant differences in overall cuticular hydrocarbon profiles compared with controls. Finally, coating healthy individuals with extracts containing cuticular hydrocarbons of immunostimulated individuals significantly increased the agonistic responses of nestmates. Conclusion: Since cuticular hydrocarbons play a critical role in nestmate recognition and other social interactions in a wide variety of insect species, modulation of such chemical profiles by the activation of the immune system could play a crucial role in the social regulation of pathogen dissemination within the colony.
AB - Background: Immune response pathways have been relatively well-conserved across animal species, with similar systems in both mammals and invertebrates. Interestingly, honey bees have substantially reduced numbers of genes associated with immune function compared with solitary insect species. However, social species such as honey bees provide an excellent environment for pathogen or parasite transmission with controlled environmental conditions in the hive, high population densities, and frequent interactions. This suggests that honey bees may have developed complementary mechanisms, such as behavioral modifications, to deal with disease. Results: Here, we demonstrate that activation of the immune system in honey bees (using bacterial lipopolysaccharides as a non-replicative pathogen) alters the social responses of healthy nestmates toward the treated individuals. Furthermore, treated individuals expressed significant differences in overall cuticular hydrocarbon profiles compared with controls. Finally, coating healthy individuals with extracts containing cuticular hydrocarbons of immunostimulated individuals significantly increased the agonistic responses of nestmates. Conclusion: Since cuticular hydrocarbons play a critical role in nestmate recognition and other social interactions in a wide variety of insect species, modulation of such chemical profiles by the activation of the immune system could play a crucial role in the social regulation of pathogen dissemination within the colony.
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U2 - 10.1186/1741-7007-6-50
DO - 10.1186/1741-7007-6-50
M3 - Article
C2 - 19014614
AN - SCOPUS:57649193553
SN - 1741-7007
VL - 6
JO - BMC Biology
JF - BMC Biology
M1 - 50
ER -