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Liver sinusoidal endothelial cells undergo apoptosis during sepsis, leading to organ dysfunction. (54.13)

Noelle Hutchins, Joshua Borgerding, Chun-Shiang Chung and Alfred Ayala
J Immunol April 1, 2011, 186 (1 Supplement) 54.13;
Noelle Hutchins
1Brown University Warren Alpert School of Medicine, Providence, RI
2Rhode Island Hospital, Division of Surgical Research, Providence, RI
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Joshua Borgerding
1Brown University Warren Alpert School of Medicine, Providence, RI
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Chun-Shiang Chung
2Rhode Island Hospital, Division of Surgical Research, Providence, RI
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Alfred Ayala
2Rhode Island Hospital, Division of Surgical Research, Providence, RI
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Abstract

Sepsis is the leading cause of death in critically ill patients, and treatment options are limited. Our laboratory studies polymicrobial sepsis in murine models, and uses the liver as a model organ to investigate the disease’s pathophysiology. The liver, characterized as an immune tolerant organ, is susceptible to septic induced inflammation. We have previously reported that there is a twofold increase in the number of liver CD8+ T cells, 24 hours following cecal ligation and puncture (CLP—a surgical procedure that generates sepsis in mice). Since activated T lymphocytes must transverse the endothelium to reach the site of infection, it is possible that they directly interact with LSECs, and mediate liver injury through Fas-mediated apoptosis. This led us to hypothesize that as CD8+ T cells directly interact with LSECs, endothelial cell dysfunction occurs. Our preliminary results indicate that septic liver CD8+ T cells have cytotoxic effects on endothelial monolayer integrity, and release pro-inflammatory cytokines when directly co-cultured with CRL-2167, a murine endothelial cell line. We have also observed through flow cytometry that LSECs (CD146+/CD45- and CD31+/CD45- populations) have an increased expression of CD54 (ICAM-1), Fas, and Annexin V staining in vivo. These data suggest that CD8+ T cells directly interact with LSECs, alter the tolerance capacity of LSECs, and potentially kill LSECs through the Fas-FasL system, ultimately leading to liver organ injury in sepsis.

  • Copyright © 2011 by The American Association of Immunologists, Inc.
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The Journal of Immunology
Vol. 186, Issue 1 Supplement
April 2011
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Liver sinusoidal endothelial cells undergo apoptosis during sepsis, leading to organ dysfunction. (54.13)
Noelle Hutchins, Joshua Borgerding, Chun-Shiang Chung, Alfred Ayala
The Journal of Immunology April 1, 2011, 186 (1 Supplement) 54.13;

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Liver sinusoidal endothelial cells undergo apoptosis during sepsis, leading to organ dysfunction. (54.13)
Noelle Hutchins, Joshua Borgerding, Chun-Shiang Chung, Alfred Ayala
The Journal of Immunology April 1, 2011, 186 (1 Supplement) 54.13;
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