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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.
Insights
Bacterial infections boost beta-glucuronidase release from polymorphonuclear leukocytes (PMNs), enhancing bacterial killing. However, certain cancer drugs inhibit this release, potentially increasing infection susceptibility.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Beta-glucuronidase release from polymorphonuclear leukocytes (PMNs) is crucial for bacterial clearance and inflammatory tissue damage.
- Understanding factors influencing PMN degranulation is vital for managing infections and inflammatory conditions.
Purpose of the Study:
- To investigate the impact of various diseases and drugs on the kinetics of beta-glucuronidase release from PMNs.
- To elucidate the role of PMN degranulation in bacterial infections and its modulation by therapeutic agents.
Main Methods:
- Studied the kinetics of beta-glucuronidase release from PMNs stimulated with opsonized zymosan.
- Compared enzyme release in PMNs from children with bacterial infections, viral infections, and those undergoing specific cancer therapies.
Main Results:
- PMNs from children with bacterial infections showed significantly increased beta-glucuronidase release compared to controls.
- Viral infections led to a delayed release of beta-glucuronidase from PMNs.
- Cancer chemotherapies (6-mercaptopurine, methotrexate, vincristine) markedly diminished PMN degranulation.
Conclusions:
- Bacterial infections stimulate beta-glucuronidase release by PMNs, likely enhancing pathogen clearance.
- Cytostatic drugs used in cancer therapy inhibit lysosomal enzyme release from PMNs, potentially increasing susceptibility to secondary bacterial infections.
- Total enzyme activities remained unchanged, indicating modulation of release rather than synthesis.