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Results for “Phagocyte Bactericidal Dysfunction”

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PubMed1988

Myeloperoxidase secretion during phagocytosis: a case of a patient with impaired bactericidal activity.

We describe a case of a 5-year-old male patient with prolonged and extensive osteomyelitis of the left femur. Staphylococcus aureus was grown from blood cultures taken upon admission and also from pus drained from an incised hip joint. A defect in immune function was suspected and neutrophil function was assessed. Chemotaxis and phagocytosis were normal, but phagocytosed S. aureus were not killed as efficiently as in control neutrophils. No inherent defect in the ability of these neutrophils to generate reactive oxidants was observed, but an unusual luminol-dependent chemiluminescence response was obtained during phagocytosis of latex beads or opsonized S. aureus: This was characterized by an initial rapid, but transient increase occurring within 1 min of addition of phagocytic stimulus. Whereas during phagocytosis of latex beads by control neutrophils less than 1% of the total myeloperoxidase activity was detected extracellularly, up to 15% was released from the patient's neutrophils. We propose that release of myeloperoxidase from the patient's neutrophils during phagocytosis reduces the intraphagosomal concentration of this enzyme and thus impairs the efficiency of intracellular killing of S. aureus.

Chemotaxis, Leukocyte↗
PubMed1989

Abnormal peroxidase-positive granules in "specific granule" deficiency.

"Specific granule" deficiency (SGD) has been previously associated with lactoferrin deficiency. The antimicrobial peptides termed defensins, comprising 30% of normal primary granule proteins, have also been shown to be markedly deficient in SGD. The present study was undertaken to correlate these findings with ultrastructural morphometric analysis and peroxidase cytochemistry. Peroxidase-positive, rim-stained, large, defensin-rich dense granules, previously described as a subpopulation of azurophil or primary granules in normal neutrophils, were markedly decreased in a patient with SGD. Morphometric studies of peroxidase-positive granules indicated an average peroxidase-positive granule area (all profiles) in the patient of 0.019 +/- 0.017 micron 2 (mean +/- SD, n = 941) compared to control values from normal neutrophils of two volunteers of 0.049 +/- 0.033 micron 2 (n = 896) and 0.050 +/- 0.039 micron 2 (n = 873) (P less than 0.001 between patient and control samples). Granule histograms showed a single peak of small peroxidase-positive granules, whereas control samples contained more prominent subpopulations of larger peroxidase-positive granules. The total number of peroxidase-positive granules per 100 micron 2 of cytoplasm in the patient was 255 +/- 124 (mean +/- SD, n = 15 cell profiles), which was similar to control values of 266 +/- 63 and 212 +/- 109. Thus, the defensin deficiency in SGD is associated with a decrease in size rather than number of peroxidase-positive granules; suggesting that defensins contribute to normal peroxidase-positive granule size and that SGD is a more global granule deficiency than originally thought.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Proteins↗
PubMed1988

Effect of in vitro formed immune complexes on macrophage functions of Mycobacterium leprae infected mice.

Nonspecific macrophage functions were studied in Mycobacterium leprae infected and preformed immune complex (IC) administered normal (NI) and thymectomized/irradiated (TRI) mice at different time periods. Uninfected controls given IC were also included. Significant decrease in the chemotaxis, phagocytosis and bactericidal activities of macrophages obtained from infected groups compared to their controls were observed. Phagocytic and chemotactic activities of macrophages were normal but intracellular killing was seen to be depressed in studies conducted in normal and thymectomized immunosuppressed groups (Vaishnavi et al., 1985, Kumar et al, 1987) which were not administered with preformed IC.

Animals↗
PubMed1977

Strain variation in BCG-induced chronic pulmonary inflammation in mice. I. Basic model and possible genetic control by non-H-2 genes.

C57BL/6 mice (haplotype H-2b) responded in a dose-dependent fashion to killed BCG by marked enlargement of the spleen and lung. Neither CBA nor C3H mice (haplotype H-2k) responded to such treatment. Pulmonary inflammation in responder B6 animals was characterized by a marked chronic interstitial and alveolar granulomatous process, and was accompanied by occasional granulomata, hyperemia, and loss of architecture in the spleen. Inflammation in non-responder CBA and C3H animals was minimal in both the lung and spleen. The response does not appear to be controlled by genes within the major histocompatibility complex, but is associated with a C57 background. B10.BR mice (responder background, H-2k) were responder animals and C3H.SW mice (nonresponder background, H-2b) were nonresponders. In addition, all animals tested with a C57 background were responders even though two of these strains were not H-2b (C57BL/Ks, H-2d and C57Br/cd, H-2k). The resolution of the mechanism of genetic control of this response in mice may provide information relevant to possible genetic control of chronic pulmonary inflammation in man.

Animals↗