Objective: To study the role of macrophage inflammatory protein (MIP)-2γ in myocarditis pathogenesis in BALB/c mice. Methods: The relationship between the progression of Coxsarckie virus B3(CVB3) viral myocarditis an...Objective: To study the role of macrophage inflammatory protein (MIP)-2γ in myocarditis pathogenesis in BALB/c mice. Methods: The relationship between the progression of Coxsarckie virus B3(CVB3) viral myocarditis and experimental autoimmune myocarditis and MIP-2γ mRNA expression in mouse was studied by TaqMan real-time fluorescent quantitative RT-PCR. Results: MIP-2γ mRNA expression rose on 3 to 5 d after CVB3 infection, reached peak on 7 d, and returned to normal level until 14 d, which corresponded well with the disease course. The MIP-2γ mRNA expression level rose significantly on the day 18 d after immunization with porcine cardiac myosin, which was consistent with pathological examination. Conclusion: MIP-2γ may be involved in the pathogenesis of myocarditis.展开更多
AIM： To study the role of macrophage inflammatory protein （HIP）-2 in liver resection-induced acceleration of tumor growth in a mouse model of hepatic metastasis. METHODS： After a 50% hepatectomy, 1×10^5 CT26....AIM： To study the role of macrophage inflammatory protein （HIP）-2 in liver resection-induced acceleration of tumor growth in a mouse model of hepatic metastasis. METHODS： After a 50% hepatectomy, 1×10^5 CT26.WT cells were implanted into the left liver lobe of syngeneic balb/c mice （PHx）. Additional animals were treated with a monoclonal antibody （HAB452） neutralizing HIP-2 （PHx＋mAB）. Non-resected and non-mAB-treated mice （Con） served as controls. After 7 d, tumor angiogenesis and microcirculation as well as cell proliferation, tumor growth, and CXCR-2 expression were analyzed using in- travital fluorescence microscopy, histology, immunohisto- chemistry, and flow cytometry. RESULTS： Partial hepatectomy increased （P〈0.05）the expression of the HIP-2 receptor CXCR-2 on tumor cells when compared with non-resected controls, and markedly accelerated （P〈 0.05） angiogenesis and metastatic tumor growth. Neutralization of HIP-2 by HAB452 treatment significantly （P〈 0.05） depressed CXCR-2 expression. Further, the blockade of MIP-2 reduced the angiogenic response （P〈 0.05） and inhibited tumor growth （P〈 0.05）. Of interest, liver resection-induced hepatocyte proliferation was not effected by anti-HIP-2 treatment. CONCLUSION： HIP-2 significantly contributes to liver resection-induced acceleration of colorectal CT26.WT hepatic metastasis growth.展开更多
文摘Objective: To study the role of macrophage inflammatory protein (MIP)-2γ in myocarditis pathogenesis in BALB/c mice. Methods: The relationship between the progression of Coxsarckie virus B3(CVB3) viral myocarditis and experimental autoimmune myocarditis and MIP-2γ mRNA expression in mouse was studied by TaqMan real-time fluorescent quantitative RT-PCR. Results: MIP-2γ mRNA expression rose on 3 to 5 d after CVB3 infection, reached peak on 7 d, and returned to normal level until 14 d, which corresponded well with the disease course. The MIP-2γ mRNA expression level rose significantly on the day 18 d after immunization with porcine cardiac myosin, which was consistent with pathological examination. Conclusion: MIP-2γ may be involved in the pathogenesis of myocarditis.
基金Supported by the grants of the Research Committee the Medical Faculty of the University of Saarland,No.HOMFOR-A/2003/1
文摘AIM： To study the role of macrophage inflammatory protein （HIP）-2 in liver resection-induced acceleration of tumor growth in a mouse model of hepatic metastasis. METHODS： After a 50% hepatectomy, 1×10^5 CT26.WT cells were implanted into the left liver lobe of syngeneic balb/c mice （PHx）. Additional animals were treated with a monoclonal antibody （HAB452） neutralizing HIP-2 （PHx＋mAB）. Non-resected and non-mAB-treated mice （Con） served as controls. After 7 d, tumor angiogenesis and microcirculation as well as cell proliferation, tumor growth, and CXCR-2 expression were analyzed using in- travital fluorescence microscopy, histology, immunohisto- chemistry, and flow cytometry. RESULTS： Partial hepatectomy increased （P〈0.05）the expression of the HIP-2 receptor CXCR-2 on tumor cells when compared with non-resected controls, and markedly accelerated （P〈 0.05） angiogenesis and metastatic tumor growth. Neutralization of HIP-2 by HAB452 treatment significantly （P〈 0.05） depressed CXCR-2 expression. Further, the blockade of MIP-2 reduced the angiogenic response （P〈 0.05） and inhibited tumor growth （P〈 0.05）. Of interest, liver resection-induced hepatocyte proliferation was not effected by anti-HIP-2 treatment. CONCLUSION： HIP-2 significantly contributes to liver resection-induced acceleration of colorectal CT26.WT hepatic metastasis growth.
