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Gamma Interferon Induces Monocyte Killing of Listeria monocytogenes by an Oxygen‐Dependent Pathway; Alpha‐ or Beta‐Interferons by Oxygen‐Independent Pathways
Author(s) -
Peck Richard
Publication year - 1989
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.46.5.434
Subject(s) - monocyte , biology , interferon gamma , alpha interferon , superoxide dismutase , beta (programming language) , microbiology and biotechnology , listeria monocytogenes , alpha (finance) , cytokine , interferon , immunology , biochemistry , oxidative stress , bacteria , medicine , genetics , construct validity , nursing , patient satisfaction , computer science , programming language
Human peripheral blood monocytes purified by counterflow centrifugal elutriation were treated with recombinant interferons–‐gamma (IFN‐γ), alpha (IFN‐α), or beta (IFN‐β)–‐and tested for their capacity to kill Listeria monocytogenes. All three IFNs increased the monocyte bactericidal activity in a dose‐dependent fashion. Exogenous catalase, an inhibitor of monocyte‐generated hydrogen peroxide, did not affect bactericidal activity. However, exogenous superoxide dismutase inhibited killing by IFN‐γ‐activated monocytes, but not by IFN‐α‐ or IFN‐β‐activated monocytes. By contrast, exogenous soybean trypsin inhibitor inhibited killing by IFN‐α‐ or IFN‐β‐activated monocytes, but not by IFN‐γ‐activated monocytes. Combinations of IFN‐γ and IFN‐α resulted in no increase in bactericidal activity. Finally, treatment with IFN‐γ resulted in different receptiveness of the cell to subsequent oxidative burst‐stimulating signals than did treatment with either IFN‐α or IFN‐β. These results suggest that monocytes treated with IFN‐γ kill L monocytogenes by an oxygen‐dependent mechanism, but treatment with IFN‐α or IFN‐β elicits principally oxygen‐independent mechanisms.