The Roll Of TLR-MYD88-NF-κBP65 Signaling Pathways In Mycoplasma Pheumonia Lung Tissue Of The Mice

Objective To investigate the role of TLR-MYD88-NF-κB P65-dependent signali ng pathway in the myocardium of Mycoplasma pneumoniae model in mice with myc oplasma infection.Methods The sixty BALB/c mice,without immunity to Mycoplasma pneumonia,were randomly divided into infection group(n=40)andcontrol group(n=20),the infect ed group received nasally vaccinated Mycoplasma pneumonia bacteria.and the control group received the same amount of PBS,The histopathologic changes were observed by hematoxylin and eosin(HE)staining.Expression of TLR2,TLR4,MYD88,NF-κBP65were determined by immunohistochemistry.Results Lung Index of mice infected group(3.06±0.04)comparedwith the control group,the lung index(0.91 ± 0.03)was significantly increased,with significant differe nce(T=166.32,P<0.05).The control group with normal lung tissue biopsy,infection biopsy showed obvious inflammation,mainly alveolar structural damage,inflammatory cell infiltration.Compared withthe controlgroup(0.0026±0.00320,0.0171±0.00590,0.022±0.005,0.023±0.006),the lung tissueofmice infected with TLR2、TLR4 、MYD88、NF-κB P65 expression level of(0.07260.03758,0.0655±0.03503,0.044±0.016,0.049±0.013)w as significantly increased,thedifference was statistically significant(T=4.114,P <0.01;T=3.023,P<0.01;T=2.817,P<0.05;T=4.302,P<0.01).Conclusion 1.Thechanges of lungindex ofmice mycoplasma pneumonia and lung t issue pathological changes are consistent.2.TLR2、TLR4 involved in the pathogenesis of mycoplasmapneumonia.3.TLR2、TLR4、MYD88、NF-κB P65 gene expression dur ing startup and activate the body’s natural immunity and acquired immunity,and Myc oplasma pneumonia infection mediated inflammation plays a key role.