1887

Abstract

The oxidative metabolism (chemiluminescence and HO release) and phagocytic activity of mouse peritoneal macrophages during chronic infections induced by and more acute infections due to were studied. In infections, macrophage chemiluminescence in response to phorbol myristate acetate (PMA) was greatest at around 2 weeks, with a 1 week lag phase after infection, while the PMA-triggered HO release was markedly enhanced even 1 d after challenge, and remained high thereafter for up to 10 weeks. The pattern of changes in the phagocytic activity of host macrophages in response to latex beads during this infection resembled the pattern seen with macrophage HO release. In the infections, the PMA-triggered chemiluminescence of the host macrophages increased 4 d (in a sublethal infection) and 2 d (in a lethal infection) after bacterial challenge, whereas the PMA-triggered HO release was markedly enhanced as early as 1 d after infection and the elevated level persisted until either the bacteria were eliminated or the animals died. The patterns of changes in phagocytic activity of the host macrophages during infection at sublethal and lethal doses differed. In the former, phagocytosis was most active in the early phase of infection, with a peak around day 2, followed by a rapid decrease; in the latter, the phagocytic ability increased more slowly, and remained elevated until the animals died. The results suggest that the macrophages induced by are in a more activated state than are those induced by .

Loading

Article metrics loading...

/content/journal/micro/10.1099/00221287-132-4-1117
1986-04-01
2024-03-28
Loading full text...

Full text loading...

/deliver/fulltext/micro/132/4/mic-132-4-1117.html?itemId=/content/journal/micro/10.1099/00221287-132-4-1117&mimeType=html&fmt=ahah

References

  1. Brummer E., Morozumi P. A., Stevens D. A. 1980; Macrophages and fungi: in vitro effects of method of macrophage induction, activation by different stimuli, and soluble factors on Blastomyces.. Journal of the Reticuloendothelial Society 28:507–218
    [Google Scholar]
  2. Campbell P. B. 1979; Defective leukotaxis in monocytes from patients with pulmonary tuberculosis.. Journal of Infectious Diseases 139:409–417
    [Google Scholar]
  3. Cheers C., Pagram F. 1979; Macrophage activation during experimental murine brucellosis: a basis for chronic infection.. Infection and Immunity 23:197–205
    [Google Scholar]
  4. Cheson B. D., Christensen R. L., Sperling R., Kohler B. E., Babior B. M. 1976; The origin of the chemiluminescence of phagocytosing granulocytes. Journal of Clinical Investigation 58:789–796
    [Google Scholar]
  5. Czuprynski C. J., Campbell P. A., Henson P. M. 1983; Killing of Listeria monocytogenes by human neutrophils and monocytes, but not by monocyte- derived macrophages.. Journal of the Reticuloendothelial Society 34:29–44
    [Google Scholar]
  6. Czuprynski C. J., Henson P. M., Campbell P. A. 1984; Killing of Listeria monocytogenes by inflammatory neutrophils and mononuclear phagocytes from immune and nonimmune mice.. Journal of Leukocyte Biology 35:193–208
    [Google Scholar]
  7. Diaz P., Jones D. G., Kay A. B. 1979; Histamine-coated particles generate superoxide (0:~) and chemiluminescence in alveolar macrophages.. Nature London: 278:454–456
    [Google Scholar]
  8. Fong K. L., McCay P. B., Poyer J. L. 1978; Evidence for superoxide-dependent reduction of Fe3+ and its role in enzyme-generated hydroxyl radical formation. Chemical-Biological Interactions 15:77–89
    [Google Scholar]
  9. Halliwell B. 1978; Superoxide-dependent formation of hydroxyl radicals in the presence of iron chelates.. FEBS Letters 92:321–326
    [Google Scholar]
  10. Johnston R. B. Jr. 1978; Oxygen metabolism and microbicidal activity of macrophages.. Federation Proceedings 37:2759–2764
    [Google Scholar]
  11. Johnston R. B. Jr,, Godzik C. A., Cohn Z. A. 1978; Increased superoxide anion production by immunologically activated and chemically elicited macrophages.. Journal of Experimental Medicine 148:115–127
    [Google Scholar]
  12. Jones T., Len L. 1976; Pinocytic rates of macrophages from mice immunized against Toxoplasma gondii and macrophages stimulated to inhibit toxoplasma in vitro.. Infection and Immunity 14:1011–1013
    [Google Scholar]
  13. King G. W., Bain G., LoBuglio A. F. 1975; The effect of tuberculosis and neoplasia on human monocyte staphylocidal activity.. Cellular Immunology 16:389–395
    [Google Scholar]
  14. Mackaness G. B. 1969; The influence of immunologically committed lymphoid cells on macrophage activity in vivo.. Journal of Experimental Medicine 129:973–992
    [Google Scholar]
  15. Miles P. R., Castranova V., Lee P. 1978; Reactive forms of oxygen and chemiluminescence in phagocytizing rabbit alveolar macrophages.. American Journal of Physiology C253:C103–108
    [Google Scholar]
  16. Nathan C. F., Root R. K. 1977; Hydrogen peroxide release from mouse peritoneal macrophages. Dependence on sequential activation and triggering.. Journal of Experimental Medicine 146:1648–1662
    [Google Scholar]
  17. Nogueira N., Gordon S., Cohn Z. A. 1977; Trypanosoma cruzi: modification of macrophage function during infection.. Journal of Experimental Medicine 146:157–171
    [Google Scholar]
  18. North R. J. 1974; T cell dependence of macrophage activation and mobilization during infection with Mycobacterium tuberculosis.. Infection and Immunity 10:66–71
    [Google Scholar]
  19. Pabst M. J., Johnston R. B. Jr . 1980; Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysac- charide.. Journal of Experimental Medicine 151:101–114
    [Google Scholar]
  20. Saito H., Tomioka H., Watanabe T. 1981; H:02- releasing function of macrophages activated with various mycobacteria based on wheat germ agglutinin and phorbol myristate acetate triggering.. Journal of the Reticuloendothelial Society 29:193–204
    [Google Scholar]
  21. Tomioka H., Saito H. 1980; Hydrogen peroxide- releasing function of chemically elicited and immunologically activated macrophages: differential response to wheat germ lectin and concanavalin A.. Infection and Immunity 29:469–476
    [Google Scholar]
  22. Weinberg J. B., Misukonis M. A. 1983; Phorbol diester-induced H202 production by peritoneal macrophages.. Cellular Immunology 80:405–415
    [Google Scholar]
  23. Wing E. J. 1981; Bacillus Calmette-Guerin (BCG) decreases resistance to Listeria monocytogenes infection in mice.. Immunology 44:509–515
    [Google Scholar]
http://instance.metastore.ingenta.com/content/journal/micro/10.1099/00221287-132-4-1117
Loading
/content/journal/micro/10.1099/00221287-132-4-1117
Loading

Data & Media loading...

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error