Hepatopancreatic and intestinal inflammation is induced by lipopolysaccharide from Microcystis in common carp via the TLRs/NF-κB pathway.

During cyanobacterial bloom outbreaks in natural water bodies, large quantities of cyanobacterial metabolites can pose a serious threat to fish survival and health. However, the effects and mechanism of action of lipopolysaccharide (LPS) from cyanobacteria on fish are yet unknown. The aim of this study was to investigate the main chemical characterization of LPS isolated from the bloom-forming cyanobacterium Microcystis and to reveal the response and mechanism of the immune-related hepatopancreas and intestine tissues of common carp following oral exposure to LPS from Microcystis at a dose of 200 mg/kg. The results of biochemical assays revealed that LPS from Microcystis caused elevated transaminase activity and increased levels of inflammatory factors in fish serum and upregulated the mRNA levels of the inflammatory factors IL-1β and TNF-α in the hepatopancreas and intestine of common carp, suggesting that LPS induced an inflammatory response in the fish hepatopancreas and intestine. This was confirmed by histopathological examination, in which pathological damage to the hepatopancreatic and intestinal tracts was observed, and the intestinal permeability was altered. In addition, biochemical and molecular examination indicated that LPS might be recognized by TLRs and subsequently activate the NF-κB signaling pathway through MyD88, leading to the activation of NLRP3-mediated pyroptosis and subsequently, thereby inducing and amplifying the inflammatory response. These results suggest that the inflammatory response induced by LPS may be mediated by the TLRs/MyD88/NF-κB pathway. This study might be beneficial for preventing Microcystis LPS-induced inflammation in common carp during cyanobacterial blooms.