Defective Chemotaxis Associated with a Serum Inhibitor in Cirrhotic Patients

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Abstract
In 22 alcoholics with active liver disease, we studied neutrophilic chemotaxis, serum hemolytic complement (C) and the complement components C 1q, C 1s, C 3, C 4, C 5 and C 3 proactivator. The cirrhotic patients had marked impairment of chemotaxis, with a mean count of 35 cells per high-power field, whereas controls had 133 cells per high-power field. Normal white cells tested with patients' serum had defective chemotaxis; however, three of four patients' cells tested with normal serum had a normal chemotactic response. In 12 patients tested, C and C 3 levels were decreased. Five of six patients' serums added to normal chemotactically active serum inhibited the expected chemotactic response. Casein-induced chemotaxis, which is C independent, was also abolished by the serum of cirrhotic patients. This defective chemotaxis may help explain the increased susceptibility to infection in cirrhosis.