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The interaction between the gut and the liver plays a significant role in individual health and diseases. Mounting evidence supports that bile acids are important metabolites in the bidirectional communication between the gut and the liver. Most of the current studies on the "gut-liver axis" have focused on higher vertebrates, however, few was reported on lower invertebrates such as shrimp with an open circulatory system. Here, microbiomic and metabolomic analyses were conducted to investigate the bacterial composition and bile acid metabolism in intestine, hemolymph and hepatopancreas of Penaeus vannamei fed diets supplemented with octanoic acid and oleic acid. After six days of feeding, the bacterial composition in intestine, hemolymph and hepatopancreas changed at different stages, with significant increases in the relative abundance of several genera such as Pseudomonas and Rheinheimera in intestine and hepatopancreas. Notably, there was a more similar bacterial composition in intestine and hepatopancreas at the genus level, which indicated the close communication between shrimp intestine and hepatopancreas. Meanwhile, higher content of some bile acids such as lithocholic acid (LCA) and α-muricholic acid (α-MCA) in intestine and lower content of some bile acids such as taurohyocholic acids (THCA) and isolithocholic acid (IsoLCA) in hepatopancreas were detected. Furthermore, Spearman correlation analysis revealed a significant correlation between bacterial composition and bile acid metabolism in intestine and hepatopancreas. The microbial source tracking analysis showed that there was a high proportion of intestine and hepatopancreas bacterial community as the source of each other. Collectively, these results showed a strong crosstalk between shrimp intestine and hepatopancreas, which suggests a unique potential "intestine-hepatopancreas axis" in lower invertebrate shrimp with an open circulatory system. Our finding contributed to the understanding of the interplay between shrimp intestine and hepatopancreas in the view of microecology and provided new ideas for shrimp farming and disease control., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

As a leading cause of occupational asthma, toluene diisocyanate (TDI)-induced asthma is an inflammatory disease of the airways with one of the most significant characteristics involving inflammation, in which the receptor of advanced glycation end products (RAGE) plays an extremely important role. However, the mechanism underlying the upregulation of RAGE is still unknown. The aim of the present study was to examine whether JNK mediates β-catenin stabilization via activation of RAGE in asthma. Herein from the results by analyzing the blood from healthy donors and patients with asthma, it was found that the expression of RAGE and p-JNK is highly correlated and elevated concomitantly with the severity of bronchial asthma. Additionally, upon sensitizing and challenging the mice with TDI, we found that RAGE inhibitor (FPS-ZM1) and JNK inhibitor (SP600125) significantly reduced the TDI-induced asthma inflammation in vivo. Furthermore, SP600125 also considerably restored RAGE and p-JNK expression. Besides, the in vitro results from TDI-HSA treatment of 16HBE cells reveal that therapeutic inhibition of JNK reduced TDI driving RAGE expression and β-catenin translocation, while treatment with Anisomycin, a JNK agonist, showed the opposite effect. Moreover, genetic knockdown of RAGE does not contribute to JNK phosphorylation, indicating that JNK functions upstream of RAGE. Collectively, these findings highlight a role for JNK signaling in RAGE/β-catenin regulation and have important therapeutic implications for the treatment of TDI induced asthma., Competing Interests: Declaration of Competing Interest The authors declare that they have no competing interests., (Copyright © 2020. Published by Elsevier B.V.)