“…Many gene families were induced after E. ictaluri infection, including heat shock proteins (Song et al, 2014, 2016; Xie et al, 2015), interlekin 17 (Wang X. et al, 2014), l-rhamnose-binding lectins (Thongda et al, 2014), nitric oxide synthase genes (Yao et al, 2014), claudins (Sun et al, 2015), peptidoglycan recognition proteins (Sun et al, 2014), Rab GTPases (Wang R. et al, 2014), Rho GTPase (Tan et al, 2017), suppressors of cytokine signaling genes (Yao et al, 2015), cytochrome P450 genes (Zhang et al, 2014), serpins (Li et al, 2015), bcl-2 genes (Yuan et al, 2016), cathepsins (Geng et al, 2015; Wang et al, 2015; Dong et al, 2016), tumor suppressor genes (Mu et al, 2015), complement regulatory protein genes (Jiang et al, 2015), septins (Fu et al, 2016), chemokines (Fu et al, 2017a,b,c), galectins (Zhou et al, 2016), apolipoproteins (Yang et al, 2017), receptor tyrosine kinases (Tian et al, 2015), NF-kB related genes (Wang et al, 2017c), phosphoinositide-3-kinases (Li et al, 2016), NCK and ABI adaptor genes (Zhou et al, 2017a), JAK and STAT genes (Jin et al, 2018). These studies indicated that most of the immune related genes were involved in the E. ictaluri disease responses.…”