scholarly journals Failure of Nitro Blue Tetrazolium reduction in the phagocytic vacuoles of leukocytes in chronic granulomatous disease

1969 ◽  
Vol 48 (10) ◽  
pp. 1895-1904 ◽  
Author(s):  
David G. Nathan ◽  
Robert L. Baehner ◽  
Don K. Weaver
Keyword(s):  
Chronic Granulomatous Disease ◽  
Nitro Blue Tetrazolium ◽  
Granulomatous Disease ◽  
Blue Tetrazolium ◽  
Tetrazolium Reduction

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

Blood ◽  
1976 ◽  
Vol 48 (2) ◽  
pp. 309-313 ◽  
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.

scholarly journals Kx: its relationship to chronic granulomatous disease and genetic linkage with Xg

Blood ◽  
1981 ◽  
Vol 58 (1) ◽  
pp. 34-37
Author(s):  
P Densen ◽  
S Wilkinson-Kroovand ◽  
GL Mandell ◽  
G Sullivan ◽  
R Oyen ◽  
...  
Keyword(s):  
Chronic Granulomatous Disease ◽  
Clinical History ◽  
Good Health ◽  
Neutrophil Function ◽  
Granulomatous Disease ◽  
Gene Coding ◽  
Nitroblue Tetrazolium Reduction ◽  
Erythrocyte Surface ◽  
The Relationship ◽  
Tetrazolium Reduction

The relationship between neutrophil function and the neutrophil antigen, Kx, as well as the linkage of the gene, Xk, with Xg was examined in a kindred with X-linked chronic granulomatous disease. Four of the eight male siblings had chronic granulomatous disease by clinical history and tests of neutrophil function, and all four had Kx- negative neutrophils. The remaining four were in good health and had normal nitroblue tetrazolium reduction tests. However, one of these latter four had Kx-negative neutrophils that functioned normally. These data suggest that closely linked but distinct genes on the X chromosome code for chronic granulomatous disease and Kx. In addition, close linkage was demonstrated between Xk and Xg, a gene coding for an erythrocyte surface antigen.

scholarly journals THE EFFECT OF MENADIONE AND PHENAZINE METHOSULFATE ON THE TETRAZOLIUM REDUCTION SYSTEM UNDER HISTOCHEMICAL CONDITIONS

1964 ◽  
Vol 12 (11) ◽  
pp. 797-804 ◽  
Author(s):  
T. HASHIMOTO ◽  
J. S. KALUZA ◽  
M. S. BURSTONE
Keyword(s):  
Nitro Blue Tetrazolium ◽  
Soluble Factor ◽  
Phenazine Methosulfate ◽  
Frozen Sections ◽  
Hydrogen Acceptor ◽  
Variable Effect ◽  
Isocitric Dehydrogenase ◽  
Blue Tetrazolium ◽  
Fresh Frozen ◽  
Tetrazolium Reduction

The influence of phenazine methosulfate and menadione on the activity of DPNH- and TPNH-tetrazolium reductase, succinic, lactic, and triphosphopyridine nucleotide-linked isocitric dehydrogenase were studied with reference to applied histochemistry. Fresh frozen sections of various tissues were employed in conjunction with nitro blue tetrazolium as the hydrogen acceptor. Phenazine methosulfate was found to produce a variable effect upon staining, enhancing it or suppressing it according to incubation conditions. Suppression was most pronounced with higher concentrations. Menadione had no suppressive influence and was useful in increasing tetrazolium reduction. Its usefulness is, however, limited unless a soluble factor, possibly DT-(DPNH-TPNH)-diaphorase, can be prevented from diffusing into the medium, and "nothing dehydrogenase" is selectively inactivated.

Heterogeneity in superoxide production as measured by nitro blue tetrazolium reduction from individual PAM

1991 ◽  
Vol 260 (6) ◽  
pp. L464-L470 ◽  
Author(s):  
K. A. DiGregorio ◽  
E. V. Cilento ◽  
R. C. Lantz
Keyword(s):  
Cell Volume ◽  
Initial Rate ◽  
Single Cells ◽  
Nitro Blue Tetrazolium ◽  
Blue Tetrazolium ◽  
Cell Data ◽  
O2 Production ◽  
Cell Volumes ◽  
Tetrazolium Reduction ◽  
Small Subpopulation

Heterogeneity in superoxide (O2-.) production (as determined by the reduction of nitro blue tetrazolium to a diformazan precipitate), cell volume, and cell spreading were measured from single rat pulmonary alveolar macrophages (PAM). Of the 330 cells that produced O2-. due to stimulation by adherence, the maximum diformazan produced (MAX) varied between 1.8 and 47.2 fmol and the maximum (initial) rate of diformazan production (R) varied between 2.2 and 81.7 X 10(-3) fmol/s. Only six PAM of 336 analyzed failed to produce O2-. suggesting that O2-. production is not a specific function of a small subpopulation of PAM but rather that all PAM are capable of producing O2-.. Importantly, O2-. production by single cells showed extensive heterogeneity that did not correlate (r2 less than 0.12) with individual cell volumes, suggesting that the observed heterogeneity may not be due to differences in maturation and/or differentiation. However, when the single cell data were grouped into cell volume subfractions small but increasing linear trends (r2 greater than 0.81) in MAX and R were found. This discrepancy suggests that PAM heterogeneity in O2-. fraction cannot be estimated adequately by measurements on subpopulations of cells.

scholarly journals Variant of X-Linked Chronic Granulomatous Disease Revealed by a SevereBurkholderia cepaciaInvasive Infection in an Infant

2013 ◽  
Vol 2013 ◽  
pp. 1-5
Author(s):  
Saul Oswaldo Lugo Reyes ◽  
Nizar Mahlaoui ◽  
Carolina Prando ◽  
Lizbeth Blancas Galicia ◽  
Marjorie Hubeau ◽  
...  
Keyword(s):  
Chronic Granulomatous Disease ◽  
Burkholderia Cepacia ◽  
Recurrent Infection ◽  
Granulomatous Disease ◽  
Protein Subunits ◽  
Nitroblue Tetrazolium Reduction ◽  
Bacteria And Fungi ◽  
High Index Of Suspicion ◽  
Tetrazolium Reduction ◽  
Increased Susceptibility

Chronic granulomatous disease (CGD) is a primary immunodeficiency characterized by increased susceptibility to bacteria and fungi since early in life, caused by mutations in any of the five genes coding for protein subunits in NADPH oxidase. X-linked variant CGD can be missed during routine evaluation or present later in life due to hypomorphic mutations and a residual superoxide production. The case of a 10-month-old boy who died of pneumonia is reported. The isolation ofBurkholderia cepaciafrom his lung, together with a marginally low nitroblue tetrazolium reduction assay (NBT), made us suspect and pursue the molecular diagnosis of CGD. A postmortem genetic analysis finally demonstrated CGD caused by a hypomorphic missense mutation with normal gp91phoxexpression. In a patient being investigated for unusually severe or recurrent infection, a high index of suspicion of immunodeficiency must be maintained.

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