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Double Ig IL-1R related molecule (DIGIRR), myeloid differentiation factor 88 (MyD88), interleukin-1 receptor-associated kinase-1 (IRAK-1), tumor necrosis factor receptor-associated factor 6 (TRAF6), and Interferon-c (IFNc), are all signaling molecules involved in Toll-like receptor (TLR)-dependent inflammation. In this study, Chinese sturgeon DIGIRR, MyD88, IRAK1, TRAF6, and IFNc expression levels in immune tissues (blood, spleen, liver, head kidney and middle kidney) were upregulated in response to Citrobacter freundii infection. DIGIRR were highest in the head kidney, MyD88, IRAK1 and TRAF6 were highest in the liver, and IFNc were highest in the blood, respectively. The expression levels of DIGIRR and other genes sturgeons challenged with Plesiomonas shigelloides were similar to those challenged with C. freundii, except that DIGIRR expression was highest in the liver. Surprisingly, the expression levels of the genes after Mycobacterium marinum challenge decreased significantly, DIGIRR, MyD88, IRAK1 were lowest in the liver, TRAF6 were lowest in the blood and IFNc were lowest in the head kidney, respectively. Taken together, the expression levels of DIGIRR and other genes in Chinese sturgeon were upregulated significantly after challenge with C. freundii and P. shigelloides, but decreased significantly by M. marinum. Although their reactions varied, these findings indicate that the DIGIRR signaling pathway in Chinese sturgeon is involved the inflammatory response to diverse bacterial infection.