In the present work the expression of different families of adhesion molecules on neutrophils and endothelial cells in patients with chronic liver disease was studied in relation to the degree of hepatic insufficiency. Sixty-four patients with chronic liver disease were classified according to the modified Child-Pugh criteria into patients with Child A, B and C with and without SBP. Immuno-phenotypic characterization of LFA-1 (CD11a/CD18), Mac-1 (CD11b/CD18) and LexAg (CD15) on peripheral blood neutrophils and determination of circulating levels of sICAM-1, sE-, sL- and sP-selectin, TNF-α, IL-1β, IL-8 and ENA-78 were conducted. High levels of TNF-α, IL-1β and IL-8 were detected in different groups of patients with liver cirrhosis compared to controls. The highest values were detected among patients with Child C, specially those with SBP. The increase in these cytokines levels was mainly attributed to impaired hepatic clearance mechanism. Assessment of TNF-α and IL-8 may, thus, be used as valuable indicators for monitoring neutrophil functions in relation to the pathological staging of cirrhotic patients. In contrast, a significant decrease in the levels of ENA-78 was detected in different groups studied compared to controls and was attributed to its increased utilization or its temporal expression and secretion in sites of inflammations. A marked elevation in serum levels of sE-, sL- and sP-selectin and ICAM-1 was also found in patients with liver cirrhosis compared to healthy subjects. Moreover, a progressive increase in the surface expression of LFA-1 (CD11a/CD18) and Mac-1 (CD11b and CD18) on peripheral blood neutrophils, which parallel the progress of the disease, was detected in cirrhotic patients. These findings indicate that increased expression of LFA-1 and up regulation of Mac-1 on neutrophils were correlated to the inflammatory process and matched the disease activity. The increased expression of β2 integrin on surface of peripheral blood neutrophil may lead to increase adhesion between the neutrophil themselves, thus contributing to cell loss and spread of microbial infection. Accordingly, the increased surface expression of Mac-1 on peripheral blood neutrophils in patient with liver cirrhosis may be used as an index of adhesive function and state of neutrophil activation. In conclusion, the simultaneous elevation in the levels of soluble adhesion molecules associated with an increase in the surface expression of β2 integrin in patients with liver cirrhosis is compatible with an activation state of endothelium (increased of E-selectin, P-selectin and ICAM-1 levels), leucocytes (increased L-selectin levels) and possibly platelets (increased P-selectin levels). This persistent activation of endothelium and leucocytes may promote a favorable environment for leucocytes migration towards the location of inflammation even in absence of infection. SBP may represent a local failure to overcome a small bacterial inoculum in the peritoneal cavity because of abnormalities in the initiation of the local inflammatory response. Evidence of neutrophil involvement in patients with chronic liver disease provide a rational for using therapies that prevent neutrophil recruitment to the liver in these patients.