Pleiotropic immunoregulation by growth‐blocking peptide in Ostrinia furnacalis
Insects rely on their innate immune system to eliminate pathogenic microbes. As a system component, cytokines transmit intercellular signals to control immune responses. Growth‐blocking peptide (GBP) is a member of the stress‐responsive peptide family of cytokines found in several orders of insects,...
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Veröffentlicht in: | Insect molecular biology 2024-06, Vol.33 (3), p.270-282 |
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Sprache: | eng |
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Zusammenfassung: | Insects rely on their innate immune system to eliminate pathogenic microbes. As a system component, cytokines transmit intercellular signals to control immune responses. Growth‐blocking peptide (GBP) is a member of the stress‐responsive peptide family of cytokines found in several orders of insects, including Drosophila. However, the physiological role of GBP in defence against pathogens is not thoroughly understood. In this study, we explored the functions of GBP in a lepidopteran pest, Ostrinia furnacalis. Injection of recombinant O. furnacalis GBP (OfGBP) precursor (proGBP) and chemically synthesised GBP significantly induced the transcription of antimicrobial peptides (AMPs) and other immunity‐related genes including immune deficiency (IMD) and Dorsal. The level of OfGBP mRNA was upregulated after bacterial infection. Knockdown of OfGBP expression led to a decrease in IMD, Relish, MyD88 and Dorsal mRNA levels. OfGBP induced phenoloxidase activity and affected hemocyte behaviours in O. furnacalis larvae. In summary, GBP is a potent cytokine, effectively regulating AMP synthesis, melanization response and cellular immunity to eliminate invading pathogens.
Ostrinia furnacalis growth‐blocking peptide (OfGBP) induces the expression of antibacterial peptides by regulating both the immune deficiency and Toll pathways and contributes to defending against bacterial infection.
OfGBP regulates the expression of prophenoloxidase 2 and induces the phenoloxidase activity.
OfGBP up‐regulates Ca2+ signals and activates the cellular immune response to eliminate pathogen invasion. |
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ISSN: | 0962-1075 1365-2583 |
DOI: | 10.1111/imb.12898 |