With the improvement of the breeding model and the improvement of feeding and management technology, it seems that the frequency of bursitis has decreased in recent years, resulting in people not paying much attention to preventing and controlling this disease during breeding and production. In fact, the incidence of bursitis in chickens has always been high.
With the rapid rise in the emergence of bacterial strains resistant to multiple classes of antimicrobial agents, there is an urgent need to develop novel antimicrobial therapies to combat these pathogens.
TFF3 rapid responds to injury, and it can reduce intestinal epithelial permeability by regulating tight junctions (FIG.2), an effect that can be attenuated by inhibition of the PI3K/AKT signaling pathway. In addition, the process of restitution requires TFF3 to act as a motogen, by promoting epithelial cell elongation and migration to cover the exfoliated surface.Studies have shown that TFF3 treatment enhances the collective migration of IEC-18 cells and forms continuous sheets of migrating cells to ensure precise coverage of the re-populated area. It is suggested that TFF3 may promote intestinal mucosal reconstitution through crosstalk between ERK and JAK/signal transducer and activator of transcription (STAT3) pathways.
The trefoil factor family (TFF) is a relatively new family of polypeptides with a three-loop trefoil domain. They are mainly synthesized and secreted by the protein-secreting epithelial cells of the gastrointestinal mucosa and are closely related to mucins. Their abundant expression in different patterns under normal conditions, physiological state under different ulcer conditions and ectopic expression suggest that they play an important role in mucosal defense and repair.
Studies have found that when animals are infected or attacked by pathogenic microorganism, the corresponding secretion of antimicrobial peptides in the body will increase sharply (100-1000 times) to fight inflammation.