Mice Macrophages Ulinastain Severe Pulmonary Infections Of Immunocompromised

Background Excessive inflammation under immunosuppression conditions is complicated in pathogenesis and often results in high fatality rate. Clinically, it is a kind of common severe and acute disease coming after transplantation.Various influential factors inside and outside of the lung will result in the release of all kinds of inflammatory mediators. As an important cell for regulating inflammatory reaction, macrophage subsets will secrete different cytokines and chemokines during the inflammatory reaction process, which leads to Cytokine Storm and increasingly severe inflammatory reaction. Functioning as the initiating cell of Cytokine Storm, macrophage participates in the subsequent excessive inflammatory reaction directly or indirectly. The inflammatory reaction, during which the body functions are out of control, will lead to vicious circle which worsens damage to bodies. Objectives to observe the effect of UIT on macrophage in BALF and pulmonary tissues of immunocompromised mouse with severe pulmonary infection(ALR), and probe into the anti-inflammatory mechanism of UIT. Methods 30 male Balb / c mice were randomly divided into Control Group, ALR Group and UIT+ALR Group, with10 mice in each group. The model of immunocompromised mouse with acute lung injury was prepared with methylprednisolone and endotoxin, followed by intervention treatment with UTI. Respiratory rate(R) of mice in each group was examined respectively 3h and 6h following the intratracheal administration. At 6hours after the intratracheal administration, the mice were narcotized with urethane and then killed and collected. Next the number of alveolar macrophage and neutrophil in BALF was detected, pulmonary tissue slice and HE staining were conducted to observe the pathological changes, positive expression of CD163 in pulmonary tissue was detected with immunohistochemistry, real-time quantitative PCR test on mRNA expression of Ml-type markers(TNF-α, IL-6,INOS) in BALF was carried out, and real-time PCR test on mRNA expression of M2-type markers(CD206, Arg-1, IL-10) in BALF was conducted. Result(1)The model group than in the control group of mice rapid shallow breathing.Occasionally appear nod breathing, respiratory distress phenomenon, respiratory rate, Ulinastatin group than in the untreated group of mice breathing gently,Occasional shortness of breath, steady breathing and downs, respiratory rate slows down(P <0.05).(2) The general concept of lung tissue: Group of lung tissue surface is soft, elastic good, Tissue density, encapsulated smooth, light red color; Model of lung tissue diffuse large area of bleeding. tissue swelling,uneven color. Ulinastatin lung tissue swelling congestion, But to a lesser degree compared with the model group. No large areas of hemorrhage, scattered bleeding.(3) The pathological changes in the lung tissue: The normal control group alveolar lung tissue thin walls, Alveolar space and alveolar no inflammatory cell accumulation, infiltration, Lung tissue was no significant rupture blood vessels, dilated; Model severely damaged lung tissue, Alveolarwall rupture, collapse, alveolar lot of red blood cells, inflammatory cell infiltration, alveolar structure disappeared even. Alveolar edema, interstitial lung widened; Ulinastatin lung tissue lesions lighter than the model group, but there are alveolar structure is incomplete, alveolar inflammatory cell infiltration and other changes.(4) The model group compared with the control number of macrophages and neutrophils in BALF increased reduction in the Ukrainian Division of macrophages and the number of neutrophils his small group compared with model group, the difference was statistically significant(P<0.05).(5) the model group than the control group, the expression of CD163 positive rate of lung tissue increased(P <0.05).(6) the model group than the control group in BALF Ml-type markers(TNF-α, IL-6, INOS) mRNA expression were increased(P <0.05). Expression Ulinastatin group compared with the model group in BALF Ml-type markers(TNF-α, IL-6, INOS) mRNA were reduced in a statistically significant difference(P <0.05). Model group than the control group, the expression of M2-type markers in BALF(CD206, Arg-1,IL-10) of mRNA were increased(P <0.05); Expression Ulinastatin group compared with the model group in BALF M2-type markers(CD206, Arg-1,IL-10) mRNA were increased in a statistically unsignificant difference(P >0.05);Conclusion(1) UTI is able to improve lung injuries to some extent and protect pulmonary tissues of immunocompromised mouse with acute lung injury.(2) Ulinastatin through the role of toxins in the immunocompromised mice infected lung macrophages play a role in anti-inflammatory.(3) Ulinastatin lung protection mechanisms within the immunocompromised mice infected with the toxin may regulate macrophage M1 / M2 cell balance, and thus play its anti-inflammatory effects.The conclusion of this experiment can be treated forfuture clinical transplantation in patients with severe pulmonary infection provide a theoretical basis.