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Study on Infection of Human Macrophages with gp120 HIV Envelope Glycoprotein and Mycobacterium Tuberculosis

Author: WangPing
Tutor: ZhangWanJiang
School: Shihezi University
Course: Pathology and Pathophysiology
Keywords: HIV viral envelope protein gp120 BCG H37Ra Human macrophages
CLC: R378
Type: Master's thesis
Year: 2009
Downloads: 24
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Abstract


Objective: To establish and to study gp120 and Mycobacterium tuberculosis infection of human macrophage model provides a theoretical basis for synergistic or enhanced Mycobacterium tuberculosis pathogenic mechanism for the HIV virus. Method: 1. Using electron microscopy Comparative Study of gp120 and international standards of BCG and M. tuberculosis strains H37Ra strains, respectively, and the dynamic process of co-infection of human macrophages, macrophages ultrastructure phase change and its differences . Using the MTT assay, nitrate reductase method, 4 - the aminoantipyrine Pyrazoline law, CFU count Comparative Study of the various groups that macrophage survival at each time point, the ability to produce NO, acid phosphatase activity and the ability of bacteria to survive within macrophages. Results: 1 gp120 may exacerbate the destructive effects of the ultrastructure of macrophages, macrophage role in the resistance against Mycobacterium tuberculosis (P lt; 0.05); BCG, H37Ra and gp120 were infected macrophages can enhance the activity of acid phosphatase, and gp120 infected macrophages with BCG, gp120 and H37Ra group, acid phosphatase activity of macrophages is lower than BCG, H37Ra singly infected macrophages group (P lt; 0.05); BCG, the H37Ra and gp120 were infected macrophages can cause a large number of macrophages in the synthesis and release of NO; ??gp120 co-infection with BCG, gp120 and H37Ra macrophages of NO synthesis and release was significantly lower than the BCG, H37Ra and gp120 Solo macrophage infection group (P lt; 0.05); With the prolongation of the time of infection, the survival rate of each group macrophages were decreased to reduce the gp120 destruction of macrophages co-infected with BCG, gp120 and H37Ra particularly severe (P lt; 0.05); BCG or H37Ra with the extension of the time of infection, the number of cells increased (P lt; 0.05), the number of bacteria in the cell gp120 with BCG or gp120 and H37Ra infection BCG or H37Ra infection alone group (P lt; 0.05). Conclusion: BCG, H37Ra and gp120, infected macrophages can be activated macrophages, enhance the activity of acid phosphatase, activated macrophages can produce large amounts of NO enhance macrophage killing action of microorganisms; gp120 can directly broken ring structure of the macrophage, to reduce macrophage acid phosphatase activity, affecting the synthesis and release of NO, weaken the role of the macrophage killing microorganisms; survival and reproduction of bacteria in macrophages led to the destruction of the cell death, BCG or H37Ra macrophages, the virulence the gp120 can improve BCG or H37Ra, to enhance BCG or H37Ra pathogenic virulence of macrophages.

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