Quantitation of superoxide production in human polymorphonuclear leukocytes from normals and 3 types of chronic granulomatous disease

Serum from most normal persons contains specific antibodies which react with common bacterial species preparing their surfaces so that phagocytosis by leukocytes can take place. The Fab part of these antibodies reacts with immunologic specificity with antigens on the surface of bacteria. Another part of the immunoglobulin molecule termed the Fc portion is activated during the attachment of the Fab portion to bacteria and becomes a site for attachment of bacteria to receptors on the surface of phagocytic cells. This activity is greatly amplified by heat-labile serum factors. Normally bacteria are rapidly killed by human polymorphonuclear leukocytes after engulfment occurs. However staphylococci and gram-negative species of bacteria survive in the leukocytes of patients with the syndrome "Chronic Granulomatous Disease of Childhood." These patients have suffered recurrent severe infections with bacterial species that are part of the body's resident bacterial flora. By contrast these patients are not at increased risk to infection from such pyogenic bacterial species as group A streptococci or pneumococci. The leukocytes from patients with chronic granulomatous disease produce little hydrogen peroxide during phagocytosis. Catalase-producing staphylococci and gram-negative bacteria are not killed, but hydrogen peroxide-producing streptococci and pneumococci are killed. A normal metabolic response to phagocytosis as well as release of lysosonial factors are essential for the bactericidal activity of human polymorphonuclear leukocytes.

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The biochemical basis of nitroblue tetrazolium reduction in normal human and chronic granulomatous disease polymorphonuclear leukocytes

Blood ◽

10.1182/blood.v48.2.309.bloodjournal482309 ◽

1976 ◽

Vol 48 (2) ◽

pp. 309-313 ◽

Cited By ~ 2

Author(s):

RL Baehner ◽

LA Boxer ◽

J Davis

Keyword(s):

Chronic Granulomatous Disease ◽

Polymorphonuclear Leukocytes ◽

Nitroblue Tetrazolium ◽

Granulomatous Disease ◽

Biochemical Basis ◽

Nitroblue Tetrazolium Reduction ◽

Normal Human ◽

Nbt Reduction ◽

Human Polymorphonuclear Leukocytes ◽

Tetrazolium Reduction

Normal human polymorphonuclear leukocytes (PMN) placed in anaerobic chambers reaching pO2's of less than 5 mm Hg fail to generate O2-, iodinate ingested particles, and stimulate glucose-1–14C oxidation through the hexose monophosphate shunt. The observation that anaerobic cells are incapable of generating O2- or reducing nitroblue tetrazolium (NBT) to formazan supports the idea that NBT reduction in phagocytizing PMN is due exclusively to oxygen-dependent O2- generating oxidase which is deficient in chronic granulomatous disease leukocytes, despite their hyperphagocytic capacity.

Download Full-text

The biochemical basis of nitroblue tetrazolium reduction in normal human and chronic granulomatous disease polymorphonuclear leukocytes

Blood ◽

10.1182/blood.v48.2.309.309 ◽

1976 ◽

Vol 48 (2) ◽

pp. 309-313 ◽

Cited By ~ 180

Author(s):

RL Baehner ◽

LA Boxer ◽

J Davis

Keyword(s):

Chronic Granulomatous Disease ◽

Polymorphonuclear Leukocytes ◽

Nitroblue Tetrazolium ◽

Granulomatous Disease ◽

Biochemical Basis ◽

Nitroblue Tetrazolium Reduction ◽

Normal Human ◽

Nbt Reduction ◽

Human Polymorphonuclear Leukocytes ◽

Tetrazolium Reduction

Abstract Normal human polymorphonuclear leukocytes (PMN) placed in anaerobic chambers reaching pO2's of less than 5 mm Hg fail to generate O2-, iodinate ingested particles, and stimulate glucose-1–14C oxidation through the hexose monophosphate shunt. The observation that anaerobic cells are incapable of generating O2- or reducing nitroblue tetrazolium (NBT) to formazan supports the idea that NBT reduction in phagocytizing PMN is due exclusively to oxygen-dependent O2- generating oxidase which is deficient in chronic granulomatous disease leukocytes, despite their hyperphagocytic capacity.

Download Full-text