Über den Verlauf der oxydativen und glykolytischen Prozesse in den Leukocyten des entzündeten Gewebes während der Phagocytose

Ado, A. D.

doi:10.1007/bf02610502

Cited by 15 publications

(4 citation statements)

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“…There remains the question of how the leucocytes obtain the necessary energy for the phagocytic activity under these conditions. Similar observations had been made by others (34,35). It is interesting to note that exudate leucocytes of guinea pigs have been reported to lose some of their cellular glycogen during phagocytosis but not during undisturbed respiration when suspended in serum (36).…”

Section: Phagocytosis Causes An Increase In the Rate Of Respiration Osupporting

confidence: 91%

Studies on the Interaction Between Phagocytes and Tubercle Bacilli

Stähelin

Suter

Karnovsky

1956

The Journal of Experimental Medicine

100

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In the tissues of a susceptible host tubercle bacilli are rapidly phagocytized by polymorphonuclear leucocytes at first and later by ceils of the reticuloendothelial system; i.e., the alveolar phagocytes in the lung and macrophages proper in other tissues (1-3). There is no doubt that the tubercle bacillus retains its vitality and ability to multiply during its residence in leucocytes and macrophages (4), but information is not available on the metabolic state of the bacilli after phagocytosis. The intracellular environment could affect the bacilli in several ways: the phagocytic enzymes could alter the physical and chemical integrity of the bacillus resulting in its destruction, or the intracellular environment could merely modify metabolic pathways or rates. For a study of the metabolic fate of tubercle bacilli within phagocytes, techniques had to be developed which would allow one to differentiate between the metabolic activities of the host cell and of the parasite. The use of tubercle bacilli labeled with radioactive carbon has been helpful in such studies. However, it was necessary first to have specific information on the metabolism of the phagocytes under the conditions employed in these experiments, since the phagocyte constitutes the environment of the engulfed parasite.In this paper experiments on the energy-yielding metabolism of polymorphonuclear leucocytes 1 and monocytes 2 will be reported, and some of the

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Section: Phagocytosis Causes An Increase In the Rate Of Respiration Osupporting

confidence: 91%

Studies on the Interaction Between Phagocytes and Tubercle Bacilli

Stähelin

Suter

Karnovsky

1956

The Journal of Experimental Medicine

100

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“…Polymorphonuclear leucocytes activated by phagocytic and chemotactic stimuli undergo a respiratory burst (Baldridge & Gerald, 1933;Ado, 1933) leading to the formation of oxygen radicals and other reactive oxygen metabolites (Babior et al, 1973;Weening et al, 1975). We have recently reported two distinct mechanisms for activation of reactive oxygen metabolite generation in polymorphonuclear leucocytes (Hallett & Campbell, 1983).…”

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confidence: 99%

Inhibition by adenosine of reactive oxygen metabolite production by human polymorphonuclear leucocytes

Roberts¹,

Newby²,

Hallett³

et al. 1985

Biochemical Journal

105

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The stimulation of reactive oxygen metabolite production from human polymorphonuclear leucocytes by chemotactic peptide (fMet-Leu-Phe) was inhibited by adenosine with a K0.5 of 0.6 microM. Dipyridamole (0.1 microM), an inhibitor of adenosine uptake, did not prevent the effect of adenosine. Non-metabolizable analogues could substitute for adenosine in the potency order N-ethoxycarboxamideadenosine greater than 2-chloroadenosine greater than adenosine greater than L-N6-(phenylisopropyl)adenosine = D-N6-(phenylisopropyl)adenosine, which is characteristic of an A2 adenosine receptor. The effects of adenosine, 2-chloroadenosine and N-ethoxycarboxamideadenosine were reversed by 8-phenyltheophylline. When endocytosis was inhibited with cytochalasin B, cells were still susceptible to adenosine receptor agonists. 2-Chloroadenosine (10 microM) reduced the activation of respiration in response to chemotactic peptide from 3.3-fold to 1.4-fold. Activation of reactive oxygen metabolite production in response to latex beads was not reversed by adenosine or its analogues. It was concluded that adenosine acts at an A2 adenosine receptor to antagonize the activation of polymorphonuclear leucocytes by those stimuli, such as chemotactic peptide, which cause an increase in the intracellular free Ca2+ concentration.

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“…It has been known for 50 years that phagocytic stimulation of PMN results in a burst of oxygen consumption (Baldridge & Gerald, 1933; Ado, 1933). This 'oxygen burst' is not due to increased mitochondrial respiration, as it is resistant to cyanide poisoning (Becker et al, 1958;Sbarra & Karnovsky, 1959), but the result of the production of oxygen radicals such as 02-, OH', '02, H202 and OC1-.…”

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confidence: 99%

Two distinct mechanisms for stimulation of oxygen-radical production by polymorphonuclear leucocytes

Hallett¹,

Campbell²

1983

Biochemical Journal

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Oxygen-radical production stimulated from rat polymorphonuclear leucocytes by either unopsonized latex particles (diameter = 1.01 microM) or chemotactic peptide (N-formyl-Met-Leu-Phe) was monitored by using luminol-dependent chemiluminescence. Azide inhibited by more than 80% the luminescence response induced by chemotactic peptide whether added before or after stimulation. However, the luminescence response to latex particles was progressively less susceptible to azide inhibition if the azide was added after the stimulus. Cytochalasin B, which was shown to abolish phagocytosis of the latex beads, also abolished the chemiluminescence response. However, the same cells showed a greatly enhanced response to chemotactic peptide. Cytochalasin B-treated cells secreted approx. 45% of total cellular myeloperoxidase in response to chemotactic peptide, but there was no detectable secretion in response to unopsonized latex particles. Microperoxidase equivalent to 20% of cellular peroxidase activity added to the cells before addition of the stimulus had no effect on the response to latex particles but increased approx. 2-fold the peak rate of chemiluminescence induced by chemotactic peptide. It was concluded that the unopsonized latex particles stimulated oxygen-radical production by the mechanism that involved endocytosis, whereas chemotactic peptide stimulated production by a mechanism that involved exocytosis of myeloperoxidase, the latter mechanism requiring an increase in intracellular free [Ca2+].

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Über den Verlauf der oxydativen und glykolytischen Prozesse in den Leukocyten des entzündeten Gewebes während der Phagocytose

Cited by 15 publications

References 0 publications

Studies on the Interaction Between Phagocytes and Tubercle Bacilli

Studies on the Interaction Between Phagocytes and Tubercle Bacilli

Inhibition by adenosine of reactive oxygen metabolite production by human polymorphonuclear leucocytes

Two distinct mechanisms for stimulation of oxygen-radical production by polymorphonuclear leucocytes

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