MicroRNAs reshape the immunity of insects in response to bacterial infection

Abstract

The interaction between bacteria and insects can significantly impact a wide range of different areas because bacteria and insects are widely distributed around the globe. The bacterial-insect interactions have the potential to directly affect human health since insects are vectors for disease transmission, and their interactions can also have economic consequences. In addition, they have been linked to high mortality rates in economically important insects, resulting in substantial economic losses. MicroRNAs (miRNAs) are types of non-coding RNAs involved in regulating gene expression post-transcriptionally. The length of miRNAs ranges from 19 to 22 nucleotides. MiRNAs, in addition to their ability to exhibit dynamic expression patterns, have a diverse range of targets. This enables them to govern various physiological activities in insects, like innate immune responses. Increasing evidence suggests that miRNAs have a crucial biological role in bacterial infection by influencing immune responses and other mechanisms for resistance. This review focuses on some of the most recent and exciting discoveries made in recent years, including the correlation between the dysregulation of miRNA expression in the context of bacterial infection and the progression of the infection. Furthermore, it describes how they profoundly impact the immune responses of the host by targeting the Toll, IMD, and JNK signaling pathways. It also emphasizes the biological function of miRNAs in regulating immune responses in insects. Finally, it also discusses current knowledge gaps about the function of miRNAs in insect immunity, in addition to areas that require more research in the future.

Keywords: host-pathogen interaction; immune pathway; innate immunity; insects; microRNAs.

Figure 1

A canonical mechanism of microRNA biogenesis and their interaction. In living organisms, primary miRNA, like other cellular transcripts, contains a 5’ cap and a polyA tail. By cleaving the stem-loop at the base of the primary miRNA, the Drosha enzyme generates the precursor miRNA. Exportin-5 subsequently transports the precursor miRNA into the cellular cytoplasm. The Dicer-1 enzyme removes the hairpin head, resulting in the development of a miRNA duplex and, in turn, the production of the RNA-induced silencing complex, in which Ago1 is one of the crucial components. The miRNA passenger strand is generally degraded, whereas the guide strand is responsible for guiding the RNA-induced silencing complex towards the target mRNA, which is bound to either the open reading frame, the 5’ Untranslated Region, or the 3’ Untranslated Region. This interaction causes mRNA degradation, translation inhibition, and, in some cases, increased mRNA stability.

Figure 2

Schematic representation of the bacterial infection route in insects and also their major immune responses to bacterial infection.

Figure 3

Schematic representation of the dysregulation of insect miRNAs in response to infection with Gram-positive or Gram-negative bacterial infection and their critical regulatory functions in the prevention of bacterial infection.

Figure 4

Representative microRNAs that control the Toll signaling pathway. Toll receptors recognize various bacterial components and either activate NF-κB signaling or induce other transcription factors via adapter molecules and downstream signaling molecules.

Figure 5

Representative microRNAs in the regulation of IMD signaling pathway. PGRP receptor recognizes different bacterial components and activates the downstream signaling cascade.