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J Leukoc Biol. 2017 Jul;102(1):127-134. doi: 10.1189/jlb.3A0716-333R. Epub 2017 May 17.

NK1.1+ cells promote sustained tissue injury and inflammation after trauma with hemorrhagic shock.

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Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Department of Biochemistry, School of Life Sciences, Central South University, Changsha, Hunan, P.R. China; and.
Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA; and.
Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA;
Clinical Translational Medical Center of Vascular Disease of the Third Xiangya Hospital, Central South University, Changsha, Hunan, P.R. China.


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-α, IFN-γ, 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.


T cell; cytokines; leukocytes; natural killer cell

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