Abstract

Fish fed a high plant protein diet exhibit intestinal inflammation, the mechanism of which needs to be clarified. We preliminarily elucidate the mechanism of the TLRs/MyD88-PI3K/Akt signalling pathway in intestinal inflammation induced by plant proteins. The diets contained 60% fish meal (FM, controls), or had 45% of the fish meal protein replaced by soybean meal (SBM), peanut meal (PM), cottonseed meal (CSM) or cottonseed protein concentrate (CPC). After an 8-week feeding trial, fish were challenged by injection of Vibrio parahaemolyticus bacteria for 7 days until the fish stabilized. The results showed that the specific growth rate (SGR) of the FM group was higher than other groups. The SGR of the CPC group was higher than those of the SBM, PM and CSM groups. The catalase (CAT) contents in the serum of fish fed a plant protein diet were higher than in FM fish. The abundances of Rhodobacteraceae and Microbacteriaceae in the MI (mid intestine) were higher in the CPC group. The TLR-2 expressions in the MI and DI of plant protein-fed fish were up-regulated. The expressions of IL-6 in the PI and MI, of hepcidin and TLR-3 in the MI, and of TLR-3 in the DI, were all lower than those of fish fed FM. In the PI, MI and DI, the protein expressions of P-PI3K/T-PI3K in the SBM and PM groups were higher than in the FM group. After the challenge, the cumulative mortalities in the FM and CPC groups were lower than those of the SBM, PM and CSM groups. These results suggested that plant protein diets reduced antioxidant capacity and glycolipid metabolism, hindered the development of the intestine and reduced intestinal flora diversity. TLR-3 is involved in the immune regulation of the PI in CPC group, MI and DI in SBM, PM, CSM and CPC groups, while might be involved in the immune regulation of the PI in SBM, PM and CSM groups. Furthermore, PI3K/Akt signaling does not participate in the regulation of PI and MI in the CSM group, MI and DI in the CPC group.

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