L selectin was blocked and hepatocellular damage after IRI was as

L selectin was blocked and hepatocellular damage after IRI was assessed to mechanistically define the role of the adhesion molecule. Results: Mice fed a HFD diet showed significant increase in body weight (42±1.2, vs. 24.6±0.6 grams; p<0.0001) and presence of hepatic steatosis by ORO stain. Splenocytes from HFD mice undergoing IRI demonstrated significant increase in CD4+ T cell activation markers, such as PD1

(p<0.0009), CD69(p<0.01), and CD62L(p<0.001), in addition to higher Venetoclax levels of serum ALT and significant increase in hepatocellular necrosis. The T cell proliferation marker Ki67 (p<0.0089), was significantly higher in HFD IRI as compared to lean IRI. Expression levels of L-selectin (p<0.03) but not P or E-selectin were elevated in HFD IRI. Increased cytokines such as IFNγ, IL-1a, IL-10, IL-6 and IL-17, suggested a pro-inflammatory milieu in HFD IRI. Blockade of L-selectin, lead to a significant attenuation of hepatocellular injury. Conclusion: A steatotic liver undergoing IRI is associated with elevation of adhesion molecule L-se-lectin along with activation and proliferation of CD4+ T cells, and a pro-inflammatory

cytokine milieu. Blocking the adhesion molecule L-selectin leads to mitigation of hepatocellular injury, thus offering an important and clinically relevant therapeutic intervention in the increasingly prevalent clinical condition of IRI of fatty liver U0126 molecular weight disease. Disclosures: The following people have nothing to disclose: Vasantha L. Kolachala, Abramowsky Carlos, Ming Shen, Alayna Feng, Allan D. Kirk,

Nitika A. Gupta “
“From the mid-1950s, it was observed that liver injury by a variety of toxins greatly sensitized the host to the effects of administered lipopolysaccharide. In the nutritional cirrhosis of choline deficiency, and in acute toxic injury as well, the need for the presence of enteric endotoxin was demonstrated. The universality of this association was striking for almost all agents associated Buspirone HCl with liver injury. In addition, the presence of endotoxemia in human liver disease was documented in the 1970s, when the hypothesis was first proposed, and correlated with the severity of the disease. Despite imposing evidence of the critical role of enteric endotoxin in liver injury, it did not excite much interest in investigators until the 1980s. With the ability to study effects of alcohol in newer delivery systems, and an increased understanding of the role of Kupffer cells in the process, the original hypothesis has been accepted. This historical review details the progress of this novel concept of disease initiation and suggests future directions to bring potential therapies to the bedside. (HEPATOLOGY 2010.) Continuing work over the past several decades has further solidified the importance of intestinal endotoxins as critical cofactors in toxic liver injury by a number of agents.

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