Innate Immune Response of <i>TmToll-3</i> Following Systemic Microbial Infection in <i>Tenebrio molitor</i>

Although Toll-like receptors have been widely identified and functionally characterized in mammalian models and <i>Drosophila</i>, the immunological function of these receptors in other insects remains unclear. Here, we explored the relevant innate immune response of <i>Tenebrio mo...

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Bibliographic Details
Main Authors: Maryam Ali Mohammadie Kojour, Ho Am Jang, Yong Seok Lee, Yong Hun Jo, Yeon Soo Han
Format: Article
Language:English
Published: MDPI AG 2023-04-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/24/7/6751
Description
Summary:Although Toll-like receptors have been widely identified and functionally characterized in mammalian models and <i>Drosophila</i>, the immunological function of these receptors in other insects remains unclear. Here, we explored the relevant innate immune response of <i>Tenebrio molitor</i> (<i>T. molitor</i>) <i>Toll-3</i> against Gram-negative bacteria, Gram-positive bacteria, and fungal infections. Our findings indicated that <i>TmToll-3</i> expression was mainly induced by <i>Candida albicans</i> infections in the fat bodies, gut, Malpighian tubules, and hemolymph of young <i>T</i>. <i>molitor</i> larvae. Surprisingly, <i>Escherichia coli</i> systemic infection caused mortality after <i>TmToll-3</i> knockdown via RNA interference (RNAi) injection, which was not observed in the control group. Further analyses indicated that in the absence of <i>TmToll-3</i>, the final effector of the Toll signaling pathway, antimicrobial peptide (AMP) genes and relevant transcription factors were significantly downregulated after <i>E. coli</i> challenge. Our results indicated that the expression of almost all AMP genes was suppressed in silenced individuals, whereas the expression of relevant genes was positively regulated after fungal injection. Therefore, this study revealed the immunological involvement of <i>TmToll-3</i> in <i>T. molitor</i> in response to systematic infections.
ISSN:1661-6596
1422-0067