The Pathogenic Investigation And TLR4Blocking Peptide Mechanism On Dairy Cattte Endometritis In Jilin

Cow postpartum endometritis is a kind of prone obstetric diseases. The disease occurs allover the world and has a history of nearly a century seriously hindered the development of animalhusbandry. In addition, it also causes serious economic loss andserious food safety problems.Though a long-time study on the disease at home and abroad, researchers found that the cowendometritis varies because of different region, different natural environment, and breedingmanagement condition of the actual situation was different. Cow postpartum uterine cavitybacteria pollution often show influence on uterine function, which is the most important reasons offalling endometritis. Although the bacteria in the uterus can get cleaned up within the first weeks,endometritis can still get persistently infected in10-17%of cows caused by bacteria endometritis.The presence of pathogenic bacteria will cause uterine endometrial inflammation and tissuedamage, delay uterine involution and affect placental survival. E. coli, a Gram-negative bacteria, isa common pathogen to cause endometritis, especially clinical endometritis. However, the actualpathophysiology remains unclear. Organisms can defense and identify the E.coli by innateimmune system then by the signal transduction pathways to induct associated immune cellactivation and cytokine secretion. Then the adaptive immune response starts to kill pathogens.Pathogen-associated molecular pattern recognition receptor can recognize pathogen invasion.TOLL-like receptors are a type of PAMP recognition receptors. TLR4recognizes bacterial cellwall components of Gram-negative bacteria-, thereby activates downstream molecules andcytokine secretion.This study found that E. coli is the main pathogenic bacteria for Clinical Endometritis in Jilinarea，as well as S.aureus、K.pneumoniae、S. dysgalactiae equisimilis、S.agalactiae、Pa.multocida、B.cereus、E.faecalis, etc. Through the analysis, we found that dominant fungi of pathogenic isE.coli、S.aureus and P. aeruginosa.After the infection by E.coli, an increased TLR4gene and protein expression was detected inthe endometria tissue of endometritis. In addition, the synthesis and secretion of proinflammatoryfactors also show an increase. A further stud have shown that after stimulation of E. coli, NF-κB and I-κB phosphorylation increased; the I-κB and NF-κB protein is promoted to dissociate,thereby reduced the inhibition. Activate NF-kB pathway to startup NF-κB p65transcription factorinto the related nucleus, inflammatory cytokine secretion.By blocking peptide detecting on TLR4different functional closed areas, the study concludedthat in the E. coli infection stage, endometrial tissue played the role of identification of E. coliTLR4. If TLR4expression is insufficient at this time, it will result in inflammatory responsereduction, bacterial destruction ability increasing, causing more serious damage.After the E. coli infection, closed TLR4downstream signaling receptor subunits, which cansignificantly reduce the NF-κB protein phosphorylation and I-κB and NF-κB protein dissociationwhich would then reduced NF-κB nucleus to startup related factor gene: consequently, TNF-α,IL-1β, IL-6and other inflammatory cytokines expression can’t be excessive. It may also preventTLR4from starting inflammatory cytokines secretion after infection, reducing inflammatoryinjury caused by excessive inflammatory cytokine which is a good protective effect to the cell.In summary, E. coli is the major pathogen of endometritis. The infection of disease processwas regulated by TLR4; TLR4stage of infection will awake the body make its recognition anddefense responses. TLR4will regulate the signaling pathway after infection, promote the secretionof inflammatory cytokines and increase the degree of inflammation.