Antibiotics and resistant genes in the gut of Chinese nine kinds of freshwater or marine fish.

Antibiotic resistance genes (ARGs) may lead to bacterial resistance and using antibiotics will promote ARGs spread. Large amounts of antibiotics were used in aquaculture, but little attention was paid to the antibiotic resistant in fish gut. In this study, nine kinds of Chinese freshwater and marine fish were acquired in a city of northern China to test the amount of antibiotics and ARGs residues in their intestinal contents. The results showed that 4 kinds of antibiotics were detected from the intestinal contents, including Doxycycline (DOX), Tetracycline (TC), Sulfamethoxazole (SMX) and Roxithromycin (ROX), and the antibiotics with the largest detected amount was ROX in Sardinops sagax (2.83 µg kg-1). Ten kinds of ARGs were detected from the intestinal contents, including strA, strB, ermB, blaTEM, oxa-30, qnrB, qnrD, sul1, sul2 and tetB, as well as one type of integron intI1. The most abundant ARGs were blaTEM. Correlation analysis showed huge difference between freshwater fish and marine fish. The results can improve our understanding of the antibiotics and ARGs residues in edible fish.

SIRT6 Acts as a Negative Regulator in Dengue Virus-Induced Inflammatory Response by Targeting the DNA Binding Domain of NF-κB p65.

Dengue virus (DENV) is a mosquito-borne single-stranded RNA virus causing human disease with variable severity. The production of massive inflammatory cytokines in dengue patients has been associated with dengue disease severity. However, the regulation of these inflammatory responses remains unclear. In this study, we report that SIRT6 is a negative regulator of innate immune responses during DENV infection. Silencing of Sirt6 enhances DENV-induced proinflammatory cytokine and chemokine production. Overexpression of SIRT6 inhibits RIG-I-like receptor (RLR) and Toll-like receptor 3 (TLR3) mediated NF-κB activation. The sirtuin core domain of SIRT6 is required for the inhibition of NF-κB p65 function. SIRT6 interacts with the DNA binding domain of p65 and competes with p65 to occupy the Il6 promoter during DENV infection. Collectively, our study demonstrates that SIRT6 negatively regulates DENV-induced inflammatory response via RLR and TLR3 signaling pathways.