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.[2]
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.
Defensins, which belongs to the host defense peptide, are defensive molecule for early defense response of mammalian mucosal immunity, and are important components of the innate immune system. Defensins not only directly kill invade pathogenic microorganisms, but also indirectly kill them by activating the immune system.
Defensins, as a natural broad-spectrum antimicrobial substance, have obvious bactericidal effects on most microorganisms in vitro and vivo experiments. However, in the vivo environment, the role of defensin can be selective.
We believe that a healthy gut is homoestasis. The early consensus is, there was a close relationship between microbiota and nutrition, but now we believe that homostasis between nutrition，microbiota and immunity is a truly stable state. And throughout gut development, immunity plays an important role in recognizing antigens and distinguishing between harmful and harmless microorganisms.
There is a significant difference between the intensive culture and natural growth, whether the animal itself, nutrition intake or external environment which are totally different. So providing beneficial substances for intestine is one way to reduce this ontological variation.
