Beta-glucuronidase release from leukocytes in children

Abstract

The release of beta-glucuronidase from polymorphonuclear leukocytes (PMNs) is important in the killing of bacteria and in producing tissue damage in acute inflammation. To investigate the effects of various diseases or drugs on degranulation, we studied the kinetics of beta-glucuronidase release from PMNs exposed to opsonized zymosan. PMNs of children with bacterial infections demonstrated increased degranulation. Within 5, 15, and 30 min the PMNs released 19 +/- 3%, 23 +/- 3%, and 26 +/- 3% of total beta-glucuronidase compared to 12 +/- 2%, 15 +/- 2%, and 16 +/- 2% of total beta-glucuronidase of control PMNs. Viral infections induced a significant delay of beta-glucuronidase release from PMNs. Maintenance therapy of acute lymphoblastic leukemia with 6-mercaptopurine and methotrexate, as well as administration of vincristine, diminished the degranulation. After 5, 15, and 30 min the PMNs released 8 +/- 1%, 10 +/- 1%, and 11 +/- 1%, as well as 6 +/- 3%, 8 +/- 2%, and 9 +/- 2% of total beta-glucuronidase. This study demonstrated that bacterial infections stimulate beta-glucuronidase release by PMNs. In contrast, cytostatic drugs inhibit lysosomal enzyme release, increasing the susceptibility to bacterial infections. The total enzyme activities were unchanged.