Abstract
Pathogen infection can cause the production of inflammatory cytokines, which are key mediators that cause the host’s innate immune response. Therefore, proper regulation of immune genes associated with inflammation is essential for immune response. Among them, microRNAs (miRNAs) as gene regulator have been widely reported to be involved in the innate immune response of mammals. However, the regulatory network in which miRNAs are involved in the development of inflammation is largely unknown in lower vertebrates. Here, we identified two miRNAs from miiuy croaker (Miichthys miiuy), miR-210 and miR-3570, which play a negative regulatory role in host antibacterial immunity. We found that the expressions of miR-210 and miR-3570 were significantly upregulated under the stimulation of Gram-negative bacterium vibrio harveyi and LPS (lipopolysaccharide). Induced miR-210 and miR-3570 inhibit inflammatory cytokine production by targeting RIPK2, thereby avoiding excessive inflammation. In particular, we found that miR-210 and miR-3570 negatively regulate antimicrobial immunity by regulating the RIPK2-mediated NF-κB signaling pathway. The collective results indicated that both miRNAs are used as negative feedback regulators to regulate RIPK2-mediated NF-κB signaling pathway and thus play a regulatory role in bacteria-induced inflammatory response.
Highlights
The innate immune system is the host’s initial defense system against the pathogens invasion
In order to investigate the miRNAs that may be involved in the regulation of RIPK2 and its signaling pathway after bacterial infection
We used miiuy croaker RIPK2-3′UTR as a query sequence to predict candidate miRNAs binding to RIPK2 through a miRNA target prediction program
Summary
The innate immune system is the host’s initial defense system against the pathogens invasion. When pathogen infects the host, pattern recognition receptors (PRRs) in the cell membrane or cytoplasm can recognize and bind to pathogen-associate molecular patterns (PAMPs) on the surface of the pathogen, thereby triggering innate immune response [1, 2]. MicroRNAs Regulate RIPK2 in Fish like receptors (NLRs) [3, 4]. NLRs as one of the important cytoplasmic PRRs, which plays a vital role in the response to various pathogen infections, such as LPS, bacterial peptidoglycan fragment muramyl dipeptide (MDP) and G-D-glutamyl-mesodiaminopimelic acid (iE-DAP) [5,6,7]. As the earliest to be studied NLR-related proteins, NOD1 and NOD2 can trigger a series of signal cascades by recruiting key adaptor protein RIPK2, thereby activating NF-kB transcription factors and promoting the production of inflammatory factors [8]. In order to ensure a moderate immune response, this signaling pathway should be precisely regulated
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