Bile acids supplementation improves colonic mucosal barrier via alteration of bile acids metabolism and gut microbiota composition in goats with subacute ruminal acidosis (SARA).

Subacute ruminal acidosis (SARA) is a common metabolic disease due to feeding high-concentrate (HC) diets to ruminants, especially dairy cows, in intensive farming system. Long term feeding HC diets commonly induce damages to hindgut barrier, leading to the translocation of harmful substances such as endotoxins (LPS) from lumen to blood, which results in a low-grade inflammation and stress response. Secondary bile acids (SBAs) play an important role in maintaining intestinal homeostasis.

Dietary bile acids supplementation improves the growth performance and alleviates fatty liver in broilers fed a high-fat diet via improving the gut microbiota.

This experiment aims to evaluate the effect of bile acids (BAs) in alleviating fatty liver disease induced by a high-fat diet (HFD) in broilers, and the modulation of the gut microbiota involved in this process. A total of 192 one-day-old Arbor Acres (AA) commercial male broilers were randomly divided into 4 groups and treated with the following diet: a basal-fat diet (BFD), a basal-fat diet plus bile acids (BFD + BAs), an HFD, and a high-fat diet plus bile acids (HFD + BAs). Bile acids were supplemented at the early growth stage (3-7 d), middle stage (17-21 d), and late stage (31-35 d).

Hcp2a of APEC affects mRNA splicing and protein quality control in DF-1 cells.

Background: Bacteria deliver effector proteins into the host cell via a secretory system that can directly act on the target to cause disease. As an important pipeline structural protein of the type VI secretion system (T6SS) complex, Hcp acts together with other virulence factors in the target cell. There is growing evidence that T6SS plays a key role in the pathogenic mechanism of APEC.

Hcp2b of T6SS affects colonization of avian pathogenic and host keratin filament expression.

T6SS (type VI secretion system) is a type of nano-syringe that exists in APEC (avian pathogenic ). Hcp (haemolysin-coregulated protein) of T6SS participates in the regulation of virulence during APEC infection. However, whether plays a role in bacterial colonization by expression in host cells remains unclear.

Hcp2a of type VI secretion system contributes to IL8 and IL1β expression of chicken tracheal epithelium by affecting APEC colonization.

Avian pathogenic Escherichia coli (APEC) is an important pathogen that causes avian colibacillosis in poultry. APEC infection can lead to pathological changes in chicken trachea. The type VI secretion system (T6SS) of APEC contribute to the pathogenicity of APEC.

Outer membrane proteins YbjX and PagP co-regulate motility in Escherichia coli via the bacterial chemotaxis pathway.

Mutation of the PhoP/Q two-component system decreases the expression of ybjX and pagP encoding outer membrane proteins, and mutation of ybjX or pagP attenuates avian pathogenic Escherichia coli (APEC) pathogenicity. However, whether ybjX/pagP mutation (double-deletion mutant) has a synergistic effect on pathogenicity remains unknown. Herein, electrophoresis mobility shift assay (EMSA) experiments showed that the PhoP/Q system regulated ybjX and pagP transcription indirectly.