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1 Systemic Inflammation Laboratory, Trauma Research, St. Joseph's Hospital, Phoenix, AZ, USA; Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA, USA
2 Systemic Inflammation Laboratory, Trauma Research, St. Joseph's Hospital, Phoenix, AZ, USA
3 Neurology and Neurosurgery Research, Barrow Neurological Institute, St. Joseph's Hospital, Phoenix, AZ, USA
* To whom correspondence should be addressed. E-mail: aromano{at}chw.edu.
The erythropoietin-producing hepatocellular (Eph) receptor tyrosine kinases and their ligands, ephrins, are involved in embryogenesis and oncogenesis by mediating cell adhesion and migration. Although ephrins can be induced by bacterial lipopolysaccharide (LPS) in vitro, whether they are involved in inflammation in vivo is unknown. By using differential mRNA display, we found that a febrigenic dose of LPS (50 µg/kg iv) induces a strong transcriptional up-regulation of ephrin-A1 in the rat liver. We confirmed this finding by real-time RT-PCR. We then quantified the mRNA expression of different ephrins and Eph receptors at Phases 1-3 of LPS fever in different organs. Febrile Phases 2 (90 min post-LPS) and 3 (300 min) were characterized by robust up-regulation (up to 16 fold) and down-regulation (up to 21 fold) of several ephrins and Eph receptors. With the exception of EphA2, which showed up-regulation in the brain at Phase 2, expressional changes of Eph receptors and eprins were limited to the LPS-processing organs: the liver and lung. Characteristic, counter-directed changes in the expressional regulation of Eph receptors and their corresponding ligands were found: up-regulation of EphA2 -- down-regulation of ephrin-A1 in the liver and lung at Phase 2; down-regulation of EphB3 -- up-regulation of ephrin-B2 in the liver at Phase 2; down-regulation of EphA1 and EphA3 -- up-regulation of ephrins-A1 and A3 in the liver at Phase 3. In the liver, transcriptional changes of EphA2 and EphB3 at Phase 2 were confirmed at the protein level. These coordinated, phase-specific responses suggest that different sets of ephrins and Eph receptors may be involved in cellular events (such as disruption of tissue barriers and leukocyte transmigration) underlying different stages of the systemic inflammatory response to LPS.
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