The Mechanism Research Of Poultry Infected With H9N2 AIV Secondary Escherichia Coli

H9N2 Subtype Avian Influenza Virus(H9N2 AIV)is a low pathogenic avian influenza virus that infects many birds and poultry and can even infect mammals,including humans and pigs.Clinically,chickens infected with H9N2 AIV exhibit severe respiratory symptoms,gastrointestinal and visceral inflammation,such as airbag and peritonitis,Mainly secondary to E.coli infection caused by,but H9N2 AIV infection secondary to the molecular mechanism of E.coli is not clear.The aim of this study was to investigate the changes of intestinal microflora,intestinal barrier and immune-related factors after infection with H9N2 AIV,and to explain the molecular mechanism of H9N2 AIV secondary to Escherichia coli in broiler chickens.Guide.In this study,16 S rRNA sequencing of the ileum and cecal contents of broilers was performed.The results showed that the intestinal flora of broiler chickens infected with H9N2 AIV was confused.The most significant changes of the cecal microflora were the major changes of the bacilli door(p<0.01).The most significant change was that the thick-walled door was significantly down-regulated(p<0.01),and the myostomyum was significantly up-regulated(p<0.01).This indicated that H9N2 AIV infected boilers could cause intestinal flora disorder.The number of Escherichia,Escherichia and Veillonella significantly increased at 5 days post-infection and 12 days post-infection from further analysis(p<0.01).However,the number Lactic acid microorganisms including Enterococcus,Lactobacillus and Streptococcus decreased inordinately.In the study,we analyzed the changes of ileal villus structure,tight junction protein,immunocytokines and Escherichia coli at 5 and 12 days after challenge.The results showed that:(1)Through the pathological sections found that 5d and 12 d after the attack of the ileal mucosa were inflammatory lesions.The ratio of villus length to depth of crypt was significantly smaller than that of blank group(p<0.05)at 5 d and 12 d after challenge,indicating that villus and crypt of ileal epithelium Suffer from varying degrees of damage.The levels of mucin TFF2 and cytoplasmic protein ZO-1 in intestinal epithelial cells were significantly decreased at 5d and 12 d after challenge(p<0.01).The mucin MUC2,occludin and Claudin-3 were also Significantly reduced(p<0.05),indicating that the ileal mucus layer structure and close connection after the attack suffered a certain degree of damage.(2)The results of Rho / Rock1/TLR-21 andTGF-β1showed that the expression of Rho did not change significantly at 5d and 12 d after challenge.The expression of Rock1 was significantly decreased at 5 days after challenge(p<0.05).The expression of TLR-21 did not change significantly at 5 days after challenge,and increased significantly at 12 days after challenge(p<0.01).The expression of TGF-β1 was significantly increased after challenge(p<0.01)on day 5 and day 12.(3)The expression of interferon-α(IFN-α)was significantly up-regulated at 5d and 12 d after challenge(p<0.05).The expression of interferon-γ(IFN-α)(p<0.01).The expression level of interleukin-15(IL-15)was significantly up-regulated at 5 days after challenge(p<0.01).The expression of interleukin-15(IL-15)(IL-17A)was significantly up-regulated at 12 days after challenge(p<0.01).The expression of IL-17 A was significantly up-regulated(p<0.05).(4)The abundance of Escherichia coli in the mycobacterium was significantly increased(p<0.01)at 5 and 12 days after challenge,all of which were more than 40%.The content of butyric acid increased significantly(p<0.05)at 5d and 12 d after challenge,which stimulated the production of E.coli toxin receptor protein(GB3).The mechanism of H9N2 AIV secondary to Escherichia coli in broiler chickens was as follows: the structure and composition of intestinal microbes in broiler chickens infected with H9N2 AIV increased rapidly,the destruction of ileal villi,the inflammatory reaction increased,the mucin layer decreased,Is conducive to Escherichia coli from the intestine attached to the mucous membrane;intestinal inflammation and make the content of butyric acid uptake,butyric acid to promote the expression of E.coli toxin receptor increased toxins easier to enter the intestinal epithelial cells,and due to intestine close connection damage Epithelial cell bypass pathway increased permeability,pathogens and toxins factors can pass through the bypass to other tissues and organs,making inflammation more serious.The inflammatory environment,in turn,further promotes the proliferation of E.Coli.