期刊
JOURNAL OF LEUKOCYTE BIOLOGY
卷 102, 期 1, 页码 127-134出版社
WILEY
DOI: 10.1189/jlb.3A0716-333R
关键词
natural killer cell; T cell; leukocytes; cytokines
资金
- National Institute of General Medical Sciences of the U.S. National Institutes of Health (NIH/NIGMS) [P50GM053789]
- National Natural Science Foundation of China [81300053]
Various cell populations expressing NK1.1 contribute to innate host defense and systemic inflammatory responses, but their role in hemorrhagic shock and trauma remains uncertain. NK1.1(+) cells were depleted by i. p. administration of anti-NK1.1 (or isotype control) on two consecutive days, followed by hemorrhagic shock with resuscitation and peripheral tissue trauma (HS/T). The plasma levels of IL-6, MCP-1, alanine transaminase (ALT), and aspartate aminotransferase (AST) were measured at 6 and 24 h. Histology in liver and gut were examined at 6 and 24 h. The number of NK cells, NKT cells, neutrophils, and macrophages in liver, as well as intracellular staining for TNF-a, IFN-g, and MCP-1 in liver cell populations were determined by flow cytometry. Control mice subjected to HS/T exhibited end organ damage manifested by marked increases in circulating ALT, AST, and MCP-1 levels, as well as histologic evidence of hepatic necrosis and gut injury. Although NK1.1(+) cell-depleted mice exhibited a similar degree of organ damage as nondepleted animals at 6 h, NK1.1(+) cell depletion resulted in marked suppression of both liver and gut injury by 24 h after HS/T. These findings indicate that NK1.1(+) cells contribute to the persistence of inflammation leading to end organ damage in the liver and gut.
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