Catfish MyD88 mediates resistance to Aeromonas hydrophila infection through coordinated IL- and IFN-dependent signaling.

As an economically important freshwater fish, catfish (Silurus asotus) has been cultivated on an increasingly large scale in recent years. However, disease outbreaks caused by bacterial pathogens have grown more severe. In this study, a pathogenic strain of Aeromonas hydrophila was isolated from diseased catfish fry. An acute toxicity assay showed that the 96-h LC50 of A. hydrophila for catfish was 1.9 × 107 CFU/mL. Experimental challenge confirmed that reinfection with this strain caused pathological damage in the intenstins, spleen, and kidney tissues. Both in vitro and in vivo experiments demonstrated that overexpression of SaMyd88 enhanced the expression of multiple immune factors, including IL6 and IFNφ1, and subsequently reduced the bacterial load of A. hydrophila. Consistently, knockdown of SaMyD88 not only suppressed inflammatory factor expression but also markedly inhibited IFN expression. Furthermore, pharmacological inhibition of IFNφ1 with GSK8612 diminished the ability of MyD88 to control A. hydrophila replication in the spleen of catfish. Together, these results indicate that MyD88 bridges IL and IFN signaling pathways to coordinate a synergistic defense against A. hydrophila infection.