Letter | Published:

Intracellular killing of Listeria monocytogenes by activated macrophages (Mackaness system) is due to antibiotic

Abstract

THE classic in vivo studies of Mackaness1 showed that the macrophage could be activated to kill intracellular organisms such as Listeria monocytogenes. This led to a series of experiments to determine the process by studying killing of this organism by macrophages both in vivo and in vitro2–6. Subsequent experiments carried out with Mackaness1 system in vitro have required antibiotic or suitable serum in the culture medium to control extracellular growth of the organism which otherwise overruns the culture7,8. Antibiotics have been shown to enter peritoneal cells9 and affect bacterial proliferation10–12, although there is evidence that the intracellular environment to some extent protects bacteria against the effects of antibiotics13,14. It has always been uncertain, therefore, whether any intracellular killing observed has been a result of antibiotic rather than activated cellular processes. Furthermore, antibiotic might be expected to enter activated cells more than resting ones, thereby causing an apparently increased intracellular killing by the former. Thus, in order to validate the system, it is necessary to prove that antibiotic is not involved in the killing of the organism. The crucial, but hitherto absent, control that is required must show true intracellular proliferation of the organism within activated cells in the face of antibiotic in the medium.

Access optionsAccess options

Rent or Buy article

Get time limited or full article access on ReadCube.

from$8.99

All prices are NET prices.

Additional information

address for reprints: Host Defence Unit, Department of Medicine, Cardiothoracic Institute, Fulham Road, London SW3, UK.

References

  1. 1

    Mackaness, G. B., J. exp. Med., 116, 381–406 (1962).

  2. 2

    Mackaness, G. B., J. exp. Med., 120, 105–120 (1964).

  3. 3

    Blanden, R. V., Mackaness, G. B., and Collins, F. M., J. exp. Med., 124, 585–600 (1966).

  4. 4

    Blanden, R. V., J. reticuloendothel. Soc., 5, 179–202 (1968).

  5. 5

    Mackaness, G. B., J. exp. Med., 129, 973–992 (1969).

  6. 6

    McGregor, D. D., Koster, F. T., and Mackaness, G. B., J. exp. Med., 133, 389–399 (1971).

  7. 7

    Wilder, M. S., and Edberg, J. C., Infect. Immun., 7, 409–415, (1973).

  8. 8

    Rhodes, M. W., and Hsu, H. S., J. reticuloendothel. Soc., 15, 1–12 (1974).

  9. 9

    Jenkins, C. R., and Benacerraf, B., J. exp. Med., 112, 403–417 (1960).

  10. 10

    Patterson, R. J., and Youmans, G. P., Infect. Immun., 1, 30–40 (1970).

  11. 11

    Simon, H. B., and Sheagren, J. N., J. exp. Med., 133, 1377–1389 (1971).

  12. 12

    Adam, D., Staber, F., Belohradsky, X., and Marget, W., Infect. Immun., 5, 537–541 (1972).

  13. 13

    Magoffin, R. L., and Spink, W. W., J. Lab. clin. Med., 37, 924–930 (1951).

  14. 14

    Shaffer, J. M., Kucera, C. J., and Spink, W. W., J. exp. Med., 97, 77–89 (1953).

  15. 15

    Bonventre, P. F., and Imhoff, J. G., Infect. Immun., 2, 89–95 (1970).

Download references

Author information

Rights and permissions

Reprints and Permissions

About this article

Further reading

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.