Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.657898
Title: Neutrophil chemotaxis in liver failure
Author: Mohamed, H. H.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 2002
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Abstract:
Neutrophil chemotaxis to IL-8 and Gro-α was reduced in patients with acute and chronic liver failure either due to alcoholic liver disease or hepatitis C compared with controls. This impairment was correlated with the severity of the disease. A partial correction in chemotaxis of patients’ neutrophils was observed after cross incubation with the control sera and vice versa using control neutrophils and patients’ sera. Neutrophil chemotaxis in patients with chronic liver failure is further reduced 2 hours after oral administration of an amino acid solution, which simulates human blood. Neutrophils isolated from the portal venous blood had similar chemotactic defects to neutrophils isolated from peripheral venous blood. However, chemotaxis was significantly reduced in neutrophils isolated from hepatic venous blood compared to neutrophils isolated from portal or peripheral blood. In cross over studies, portal neutrophil chemotaxis was significantly reduced after incubation with hepatic venous serum and vice versa. The CXC chemokines IL-8, IFN-γ-inducible protein (IP-10), and Monokine Induced by Interferon-γg (mig) were significantly elevated in patients with both acute and chronic liver failure compared with controls. There were no significant difference in neutrophil expression of both CXCR1 and CXCR2 chemokine receptors in patients with either acute or chronic liver failure compared with the controls. Neutrophil chemotaxis to CXC chemokines is impaired in patients with either acute or chronic liver failure. There is a functional defect in both CXCR1 and CXCR2 chemokine receptors. Impaired neutrophil chemotaxis may combine to the increased risk of infection in these patients. This impairment in chemotaxis may be due to CXC receptor desensitization caused by circulating humeral factor/s plus the intrinsic defect of the neutrophils.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.657898  DOI: Not available
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