O2- and H2O2 production during the respiratory burst in alveolar macrophages.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to P Bellavite.
Explore the source record for details and available documents.
The oxidative response to phagocytosis by chicken polymorphonuclear leucocytes was investigated as compared to guinea pig polymorphonuclear leucocytes. The polymorphs from both species respond to phagocytosis with an increased oxygen consumption, an increased generation of O2 and H2O2, and an increased oxidation of glucose through the hexose monophosphate shunt. The rate of oxygen consumption, and generation of O2- and H2O2 by phagocytosing chicken polymorphonuclear leucocytes is considerably lower than with phagocytosing guinea pig polymorphonuclear leucocytes. By contrast, the extent of hexose monophosphate shunt stimulation in chicken polymorphs is comparable to that of guinea pig polymorphs. Evidence is presented suggesting that H2O2 is preferentially degraded in chicken cells through the glutathione cycle, whereas catalase and myeloperoxidase are the two main H2O2 degrading enzymes in guinea pig cells. The 20,000 g fraction of the postnuclear supernatant of chicken polymorphs contains a cyanide-insensitive NADPH oxidizing activity which is stimulated during phagocytosis. Similar properties for the NADPH oxidizing activity of guinea pig polymorphs have been previously reported. It is concluded that the metabolic burst of phagocytosing chicken polymorphonuclear leucocytes is qualitatively similar to that of guinea pig polymorphonuclear leucocytes, but the latter cells are more active in all the biochemical parameters that have been measured. The difference in the H2O2 degradation pathways between the two species is accounted for by the lack of myeloperoxidase and catalase in chicken polymorphs.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In the present study we investigated the correlation between the progression of adjuvant arthritis induced by Mycobacterium butyricum and the production of nitric oxide and some pro- and anti-inflammatory cytokines in arthritic rats and in rats treated with low intra-peritoneal doses of Mycobacterium 3 and 10 days after arthritis induction. The intra-peritoneal administration of Mycobacterium antigen significantly inhibited disease development. Compared to healthy rats, a rise in serum and peritoneal pro-inflammatory cytokines was observed in all arthritic rats already from the 14 day. The treatment with intra-peritoneal Mycobacterium was associated with a significant reduction in IL-6 serum concentrations and a slight decrease of IFN-gamma production by peritoneal macrophages. Nitrite/nitrate plasma and peritoneal levels were significantly higher in all arthritic rats. Intra-peritoneal administration of Mycobacterium caused a further increase in nitrite/nitrate plasma concentrations, while no differences were evident in nitric oxide production by peritoneal macrophages. From our data it is evident that among the variables here investigated, IL-6 seems to be the more representative marker of the disease and of the treatment effect. A possible role of nitric oxide as a modulator rather than a direct mediator in this model of inflammation is discussed.
BACKGROUND: The aim of this study was to investigate some physical changes (volume, conductivity and scatter) in human polymorphonuclear leukocytes (PMN) activated with phorbol myristate acetate (PMA). METHODS: Volume changes in PMA-activated neutrophils were assayed by both STKR and STKS, two Coulter hematological analyzers. Scatter changes in PMN activated by PMA in suspensions containing nitro-blue tetrazolium (NBT) were investigated on STKS scattergrams. RESULTS: PMA activation induced PMN volumetric increases that could be assayed with STKR and displayed with STKS. The activation of PMN in suspension containing NBT induced cellular scatter changes on STKS scattergrams. The differences in scatter between resting and PMA-activated neutrophils may thus provide a semiquantitative assay of NBT reduction and superoxide production. Volume changes in PMA-activated neutrophils were due to cellular swelling through water uptake, induced by Na+/H+ antiport activation and Na+ influx. Since volume changes in PMA-activated neutrophils might occur without O2- production and vice versa, in the cases in which PMA activation of protein kinase C cannot be demonstrated by O2- production, the effect of PMA on protein kinase C- mediated Na+/H+ antiport activation, and in turn on PMA volume changes, reflects protein kinase C activation. CONCLUSIONS: A screening of neutrophils unresponsive to volumetric changes from PMA activation may be easily performed using both Coulter STKR and STKS analyzers, whereas expected or defective PMA-induced production of O2- may be semi-quantitatively evaluated by STKS.
OBJECTIVES: Several hypotheses have been proposed regarding the role of HLA-B27 antigen in the pathogenesis of the spondylarthropathies. METHODS: We studied some neutrophil functions in vivo in patients affected by ankylosing spondylitis or by reactive arthritis, with or without HLA-B27, and in healthy control subjects. In vivo neutrophil migration was investigated by Senn's skin window technique. An adhesion assay was also conducted and superoxide production was measured in circulating and migrating neutrophils after different stimuli. RESULTS: Neutrophil migration in vivo was higher in the HLA-B27 positive patients than in the controls, while no difference was found between the HLA-B27 negative patients and controls. Our data showed an increased response to formyl-methionyl-leucyl-phenylalanine by circulating neutrophils in the patients with ankylosing spondylitis, both HLA-B27 positive and negative, in comparison with all the other subjects. CONCLUSIONS: Our results revive the question of the role of HLA-B27 in the regulation of neutrophil migration; the reported in vivo priming of circulating neutrophils seems to be related to ankylosing spondylitis rather than to HLA-B27.