BACTERICIDAL FUNCTION OF HUMAN POLYMORPHONUCLEAR LEUKOCYTES

PEDIATRICS ◽  
1972 ◽  
Vol 50 (2) ◽  
pp. 264-270
Author(s):  
Paul G. Quie
Keyword(s):  
Hydrogen Peroxide ◽  
Chronic Granulomatous Disease ◽  
Polymorphonuclear Leukocytes ◽  
Bacterial Species ◽  
Bacterial Flora ◽  
Granulomatous Disease ◽  
Serum Factors ◽  
Gram Negative ◽  
Increased Risk ◽  
Human Polymorphonuclear Leukocytes

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.

STUDIES OF POLYMORPHONUCLEAR LEUKOCYTES FROM PATIENTS WITH CHRONIC GRANULOMATOUS DISEASE OF CHILDHOOD: BACTERICIDAL CAPACITY FOR STREPTOCOCCI

PEDIATRICS ◽  
1968 ◽  
Vol 41 (3) ◽  
pp. 591-599
Author(s):  
Edward L. Kaplan ◽  
Throstur Laxdal ◽  
Paul G. Quie
Keyword(s):  
Chronic Granulomatous Disease ◽  
Polymorphonuclear Leukocytes ◽  
Gram Negative Bacteria ◽  
Granulomatous Disease ◽  
Gram Negative ◽  
Modified Method ◽  
Bactericidal Capacity ◽  
Normal Manner ◽  
Streptococcal Species

Polymorphonuclear leukocytes (PMNs) from children with chronic granulomatous disease of childhood have been shown to readily phagocytize staphylococci and certain gram-negative bacteria, but they demonstrate an impaired intracellular bactericidal capacity for these organisms. The in vitro phagocytic and bactericidal capacities of PMNs from three patients with this disease for four species of streptococci (Streptococcus faecalis, Streptococcus viridans, microaerophlic streptococci, and Streptococcus pyogenes) were tested by the modified method of Maaloe. The PMNs obtained from the patients phagocytized and killed the four species of streptococci in a normal manner while still showing the defect for Staph. aureus and S. marcescens. Morphologic examination of coverslip preparations of PMNs revealed minimal post-phagocytic degranulation and vacuole formation when either staphylococci and serratia or the streptococcal species were tested. This suggests that different intracellular mechanisms may be responsible for the streptococcal killing. These observations are in accord with the clinical courses of these patients, who rarely have serious streptococcal infections in contrast to the frequent and life-threatening infections caused by staphylococci and some gram-negative bacteria.

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.

CHRONIC GRANULOMATOUS DISEASE: CORRELATION BETWEEN PATHOGENESIS AND CLINICAL FINDINGS

PEDIATRICS ◽  
1971 ◽  
Vol 48 (5) ◽  
pp. 730-739 ◽  
Author(s):  
Richard B. Johnston ◽  
Robert L. Baehner
Keyword(s):  
Hydrogen Peroxide ◽  
Chronic Granulomatous Disease ◽  
Chronic Infection ◽  
Reticuloendothelial System ◽  
Clinical Findings ◽  
Granulomatous Disease ◽  
Phagocytic Cells ◽  
Gram Negative ◽  
Serious Infections ◽  
Suppurative Lymphadenitis

Chronic granulomatous disease (CGD) results from a failure of patients' phagocytic cells to kill ingested bacteria. The inability to kill intraphagocytic microorganisms leads to granuloma formation and abscesses throughout the reticuloendothelial system. Thus, the clinical picture of CGD is characterized by suppurative lymphadenitis, hepatosplenomegaly, pneumonia, and hematologic evidence of chronic infection. The bactericidal defect which characterizes CGD phagocytes appears to be due to their inability to generate hydrogen peroxide (H2O2). The organisms which infect patients are those which require phagocytic production of H2O2 for death–staphylococci and gram-negative enterics. There are simple means of confirming a clinical diagnosis of CGD, and prolonged therapy with specific antibiotics may therefore suppress the frequency of such serious infections.

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

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.

scholarly journals Back Pain in a 23-Year-Old Male With X-Linked Chronic Granulomatous Disease

2019 ◽  
Vol 6 (11) ◽  
Author(s):  
Michelle C Sabo ◽  
Michela Blain ◽  
Denise McCulloch ◽  
Heather L Glasgow ◽  
Dhruba J Sengupta ◽  
...  
Keyword(s):  
Back Pain ◽  
Invasive Aspergillosis ◽  
Chronic Granulomatous Disease ◽  
Vertebral Osteomyelitis ◽  
Aspergillus Species ◽  
Granulomatous Disease ◽  
First Case ◽  
Increased Risk

Abstract Patients with chronic granulomatous disease are at increased risk for invasive aspergillosis. Cryptic Aspergillus species are being increasingly recognized as distinct causes of infection in this population. In this study, we describe the first case of Aspergillus udagawae vertebral osteomyelitis in a patient with X-linked chronic granulomatous disease.

STUDIES ON INTERACTION OF BACTERIA, SERUM FACTORS AND POLYMORPHONUCLEAR LEUKOCYTES IN MOTHERS AND NEWBORNS

PEDIATRICS ◽  
1969 ◽  
Vol 44 (1) ◽  
pp. 49-57 ◽  
Author(s):  
John H. Dossett ◽  
Ralph C. Williams ◽  
Paul G. Quie
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Bacterial Species ◽  
Group B Streptococcus ◽  
Newborn Infants ◽  
Maternal Serum ◽  
Humoral Factors ◽  
Serum Factors ◽  
E Coli ◽  
Serum Fractions ◽  
Group B

The bactericidal capacity of newborn infants' whole blood for E. coli was deficient compared to the mothers, and attempts were made to identify cellular or humoral factors responsible for this deficiency. Separated polymorphonuclear leukocytes from newborn infants were found to be similar to polymorphs from mothers in capacity to engulf and kill E. coli and other bacteria so that cellular deficiency was not evident. Comparison of the serum opsonic capacity of newborn infants' and mothers' sera revealed deficient opsonic capacity for E. coli in newborn sera. The mean opsonic titer for E. coli was 46.7 in mothers and 4.3 in neonates. Serum opsonic titers for Staph. aureus and group B streptococcus were similar. The opsonic capacity for all bacterial species was decreased when the sera were heated or decomplemented with immune complexes indicating the phagocytosis amplifying role of complement. The newborn-maternal difference in opsonic capacity for E. coli was presumably a result of deficient 19S antibodies, the primary opsonic antibodies for this organism. Maternal 19S serum fractions alone, however, showed no opsonic capacity for E. coli. Addition of a complement source (newborn serum absorbed with E. coli) revealed the opsonic capacity of these 19S maternal serum fractions for E. coli. Antibodies in 19S serum fractions therefore are efficient opsonins for E. coli; however, complement is necessary to demonstrate their opsonic potential.

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