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Results for “Phagocyte Bactericidal Dysfunction”

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At least 55 records · Page 3Linked to original sources
PubMed1976

Chronic granulomatous disease in an adult male: A proposed X-linked defect.

A 25-year old patient with chronic granulomatous disease of somewhat unusual history is described. The diagnosis of CGD was based on increased susceptibility to infection, granulomatous appearance of tissues, and diminished bactericidal and metabolic response of leukocytes during phagocytosis: the clinical and cellular features considered phenotypic of CGD. A 16-year-old female sibling had bactericidal and metabolic abnormalities of leukocyte function similar to those of the patient's leukocytes. Leukocytes from another sister, 26 years of age, were intermediate in bactericidal capacity. Two populations of leukocytes were identified by a histochemical test of NBT reduction. Both normal and abnormal polymorphonuclear leukocytes were present in the leukocyte population of the two sisters. Leukocytes from the patient's mother and maternal grandmother were normal by all methods tested. These findings are taken as evidence of a germ-line mutation in the chromosomal gene causing CGD, with transmission of the genetic defect from the mother to the son.

Adult↗
PubMed1977

Deficiency of NADPH oxidase activity in chronic granulomatous disease.

NADPH oxidase activity was examined in paired 27,000 x g granule fractions isolated from normal polymorphonuclear leukocytes from patients with chronic granulomatous disease. At 0.17 mM NADPH, the oxidase activity was not measurable in normal resting cells but was activated by phagocytosis. This activation was absent in CGD cells. At higher levels of NADPH, activity was present in cells from patients with CGD, although it was lower than normal, and no difference in activity was found between resting and phagocytizing cells. Granule fractions from phagocytizing normal cells exhibited higher than granule fractions from resting normal cells at all levels of NADPH. These results suggest that NADPH oxidase activity is defective in chronic granulomatous disease, and further that the defect is not the absence of the enzyme but rather a failure to activate it.

Adolescent↗
PubMed1975

Phagocytosis in patients and carriers of chronic granulomatous disease.

The phagocytic capacity of leucocytes from four patients and two carriers of chronic granulomatous disease (C.G.D.) was compared to that of normal leucocytes. Leucocytes from C.G.D. patients phagocytised more Staphylococcus aureus than did normal leucocytes after 5, 10, and 20 minutes of incubation. Phagocytosis by leucocytes from two carriers of C.G.D. was intermediate between that in the patients and in controls. In contrast, phagocytosis of Streptococcus faecalis, an organism readily killed by C.G.D. leucocytes, was similar for control and C.G.D. leucocytes. Enhanced phagocytosis may represent an attempt by leucocytes to compensate for a bactericidal abnormality. In addition, these observations may partly explain why carriers of C.G.D. are not more susceptible to infection despite abnormal leucocyte function. Detection of carriers using the described assay of phagocytosis appears relatively simple compared to previously described methods.

Blood Bactericidal Activity↗