Multiomics analyses reveal that NOD-like signaling pathway plays an important role against Streptococcus agalactiae in the spleen of tilapia

Streptococcus aglactiae(GBS) infection in tilapia is a serious global disease that causes significant production loss. Here, we studied the role of GBS in the spleen and the spleen's response against the pathogen through dual RNA-seq and proteome technology. Animals were divided into three groups: control, virulent treated (HN016), and attenuated treated (YM001). Spleen samples were collected and analysis when a disease outbreak. Dual RNA-seq result showed the virulence factor genes of GBS, included CAMP factor, PGK, OCT, enolase, scpB, Sip, bca, were upregulation. downregulation of GapA, cylE, OCT, scpB, C5AP, rlmB, hly, FBP, in HN016 and YM001. But for proteomic, OCT and bca were downregulation, the others were upregulation. For host transcriptome KEGG analysis showed, the NOD-like receptor signaling pathway (NLRs) and TOIL-like receptor signaling pathway (TLRs) were upreguoation in HN016 infected fish than the control fish; But for proteome KEGG, only the NLRS was up, the TLRS was not change. Compared with YM001 infected fishes, for transcriptome, NLRs and TLRs in infected HN016 fishes were significance rise (p < 0.01); for proteome, the NLRs was up (p < 0.05), but TLRs was no change. Analysis of pathogen-host interaction showed that the peptidoglycan (PNG), CD2, LCK, and host's Zap70 were involved in the regulation of NLRs; PNG, LCK, and ZAP70 were involved in the regulation of TRLs. Conclusion: the virulent strain HN016 and attenuated strainYM001 differed in the quantity of virulence factors. In tilapia's innate immune system, NLRs was the main defense factors, but bacteria avoided the host defense through TLRs.