![]() 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. 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. 1y Report this post Stolze printing maximizing their investment in Stahl folding equipment Meeting the customers demands with highly productive. ![]() 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. Mark Kubes Account Manager Heidelberg USA, Inc. 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. The objectives of this study were to investigate the involvement of neutrophils in Con A-induced hepatitis in vivo via intravital microscopy. 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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