In summary, the present data support the concept that neutrophils play an important and previously unrecognized role in governing Con A-induced CD4+ T cell recruitment to the liver and the subsequent development of hepatitis. Performed extensive profit and loss analysis to achieve margins. Following neutrophil depletion, a significant inhibition of Con A-induced CD4+ T lymphocyte recruitment to the liver resulted and complete reduction in hepatic injury, as assessed by serum alanine aminotransferase levels. Curtiss-Wright Controls Integrated Sensing, Inc. Using flow cytometry, we observed that Con A could bind directly to neutrophils, which resulted in a shedding of L-selectin, an increase in beta(2)-integrin expression, and the production of reactive oxidants. Furthermore, immunohistochemistry showed a significant increase in neutrophils recruited to the liver post-Con A treatment in association with liver cell damage, as reflected by elevated serum alanine aminotransferase levels. Fluorescence microscopy identified that within 4 h of Con A administration only a minority of the recruited leukocytes were T lymphocytes. After Con A administration, we observed a significant increase in leukocyte rolling flux, a decrease in rolling velocity, and an increase in leukocyte adhesion to the hepatic microvasculature. I would think that now that youve spoken to someone, this should get resolved to your satisfaction. The objectives of this study were to investigate the involvement of neutrophils in Con A-induced hepatitis in vivo via intravital microscopy. Mark Kubes has been in the same brick & mortar location for decades. In this study, we report that neutrophils are the key initiators of lymphocyte recruitment and liver injury caused by Con A. Hepatitis occurring after the administration of Con A in mice is felt to be a T lymphocyte-mediated disease. Leukocyte infiltration into the liver is paramount to the development of liver injury in hepatitis.
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