In:
European Journal of Immunology, Wiley, Vol. 20, No. 4 ( 1990-04), p. 869-873
Abstract:
Although shortly after the onset of a mycobacterial infection granulocytes are present at the site of inflammation, the role of granulocytes in the elimination of mycobacteria is not well understood. In vitro studies with, for example Mycobacterium tuberculosis or M. bovis , are hampered by the slow proliferation and clumping of the bacteria. To avoid these disadvantages, we developed a model using the atypical mycobacterium M. fortuitum . The present study concerned two questions: whether human granulocytes are able to phagocytose and intracellularly kill opsonized M. fortuitum and whether intracellular killing of these bacteria can be enhanced by treatment of the granulocytes with recombinant human interferon‐γ (rIFN‐γ). The results showed that normal granulocytes phagocytosed opsonized M. fortuitum rapidly, but did not kill these bacteria effectively. The intracellular killing of M. fortuitum was significantly enhanced by incubation of the granulocytes with rIFN‐γ for 18 h before the start of the killing assay. Since these rIFN‐γ‐pretreated granulocytes did not release more O 2 − and H 2 O 2 upon stimulation with phorbol 12‐myristate 13‐acetate or opsonized M. fortuitum than control granulocytes, non‐oxidative killing mechanisms are probably involved in the enhanced killing of M. fortuitum .
Type of Medium:
Online Resource
ISSN:
0014-2980
,
1521-4141
DOI:
10.1002/eji.1830200423
Language:
English
Publisher:
Wiley
Publication Date:
1990
detail.hit.zdb_id:
1491907-2
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