The Effect Of Endotoxin Induced By Heat Stress On Liver Injury In Broiler Chickens

Bacterial endotoxin is the composition of the outer membrane ofgram-negative bacteria cell walls,which is released when the bacteria die or growrapidly. Endotoxin can enter the body to activate the mesenchymal cells and themyeloid cells,especially can induce mononuclear cell synthesis and release various ofcytokines,growth factors,chemokines and inflammatory mediators which could causeinflammation,shock,multiple organ failure of the body and even death. It can alsodirectly effect on endothelial cells,myocardial cells,fibroblasts and parenchymalcells,causing cell damage or apoptosis.Different species of gram-negative bacterialendotoxin are roughly the same pathological changes and clinicalsymptoms.Endotoxin stability is too strong to be inactivated that it is common tocause gram-negative bacteria endotoxin blood disease in clinic. The bacteriaendotoxin pollution of surgical instrument, flushing system, lavage fluid, liquidmedicine and interventional therapy, catheter, drainage tube placement can makeanimals occur exogenous endotoxin blood disease. In addition, all kinds ofstress,trauma surgery, digestive system diseases can cause animals appear entergenousendotoxin blood disease. However, clinicians concern not enough about the damageof endotoxin in the diagnosis and treatment of animals. For example, although thebacteria is eliminated by using the antibiotics but the animals occur serious endotoxinblood diseases such as pyoderma, peritonitis, pyometra which can cause badly hurt onanimals in the treatment of gram-negative bacteria infection. So, it is necessary tocontrol the infection of bacteria.At the same time,more serious endotoxin blooddisease must be corrected in order to avoid the risk of pet death. Therefore, cliniciansmust clear the concept of “treat bacteria and endotoxin”in the diagnosis and treatmentof animal diseases.Acute heat stress often leads to the death of chickens.The entergenous endotoxinblood disease which caused by heat stress is an important factor of poultry death. Inthis test, we use AA broilers as the research object to set up the thermal stress ofendotoxin blood disease model, by using HE staining, cell microscopy, limulus test,blood biochemistry and molecular biology techniques to discuss the liver damage ofthe thermal stress of endotoxin blood disease and the expression situation of theendotoxin receptor. Meanwhile, it can also provide the basis for the endotoxin damageof animals.Along with the extension of heat stress time,the broilers appeared depressed ofspirit,asthma,diarrhea,etc. Phenomenon. Pathological histology showed that the smallintestinal villus,serous and submucosa,muscular layer have no obviously changes inthe early stage of heat stress,then the small intestinal villus occured smallfracture,capillary,intestinal villus mucosa epithelial cells fell off and intestinalstructure damaged in the later stage of heat stress.Part of liver cell nucleus dissolvedand liver blood sinus mild expansion at the early time.However,it became worse suchas hepatocellular fatty degeneration,liver blood sinus expansion,liver cellsdisorganized and inflammatory cells infiltration. The results of limulus test show that, The blood endotoxin levels of broiler chickensraised at the prime phase of heat stress;Blood endotoxin level was up to7times higher thanthe control group at the later phase of heat stress.It proved that, broiler intestinal mucousmembrane was injury at the acute heat stress,intestinal endotoxin enter into the circulation and theendotoxin levels raised.The theory of endotoxemia occurred in broilers under heat stress has beenverified.There was no significant different between VC group and test group.Microscopic examination of blood cells showed that the number of red blood cellsincreased slightly at the early phase of heat stress endotoxemia,and decreasedsignificantly at the later phase,there were not significant different between the twogroups including the VC group and the test group.However,the leukocytes decreasedsignificantly at the early phage of heat stress endotoxemia, then it increasedsignificantly,heat stress endotoxemia reduces the immunity of broilers, the broilers was in astate of stress status.VC failed to improve heat stressed broilers the endotoxin immuno-compromised status.The results of blood biochemical showed that the main indicators as ALT continued torise,there was a extremely significant different than control group.Liver tissues of broilers wasdamaged under heat stress,the liver function was affected.At the same time, another reason forblood endotoxin increasing was that liver function of broiler was damaged and endotoxin removalmechanism was failure.The results of RT-PCR technology on liver endotoxin receptor detection showthat,the expression levels of TLR4receptor mRNA raised at early phase of heatstress,the expression increased to1.4times that of the control group at later phase of heatstress,there was a significant different than control group.Activation of TLR4receptorsthrough NF-κ B induced the producing of a great deal of inflammatories,induced thesystemic inflammatory response syndrome (SIRS)、 disseminated inravascularcoagulation（DIC）、septic shock and multiple organ failure (MODF),This may be thereason for the massive death of acute heat stress broilers.From all above we can include that heat stress can lead to the intestinal injury ofbroilers then appear the endotoxin blood disease, and become more and more worseduring the extension of heat stress time. Enterogenous endotoxin blood diseaseincrease the mRNA expression level of liver’s TLR4receptor. The inflammationinduced by endotoxin exacerbate the liver damage.So we should not only payattention to prevent the occurrence of oxidative stress, but also pay more attention tostrengthen nutrition, protect the gut barrier, correction of endotoxin blood disease forpreventing the heat stress.From all above we can include that heat stress can lead to the intestinal injury ofbroilers then appear the endotoxin blood disease, and become more and more worseduring the extension of heat stress time. Enterogenous endotoxin blood diseaseincrease the mRNA expression level of liver’s TLR4receptor. The inflammationinduced by endotoxin exacerbate the liver damage.So we should not only payattention to prevent the occurrence of oxidative stress, but also pay more attention tostrengthen nutrition, protect the gut barrier, correction of endotoxin blood disease forpreventing the heat stress.