In vitro activation of mouse neutrophils by recombinant human interferon-gamma: Increased phagocytosis and release of reactive oxygen species and pro-inflammatory cytokines
In vitro activation of mouse neutrophils by recombinant human interferon-gamma: Increased phagocytosis and release of reactive oxygen species and pro-inflammatory cytokines
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DOI:
10.1016/j.intimp.2013.12.010
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发表时间:
2014-02-01
影响因子:
5.6
通讯作者:
Mantovani, B.
中科院分区:
文献类型:
--
作者:
Marchi, L. F.;Sesti-Costa, R.;Mantovani, B.
Here, we investigated the ability of IFN-gamma to modulate the functions of mouse neutrophils in vitro. Neutrophils incubated in the presence of IFN-gamma showed enhanced phagocytosis in response to zymosan, opsonized zymosan or precipitated immune complexes of IgG and ovalbumin. The effect of IFN-gamma was dose-dependent with an initial response at 10 U/ml and a maximal response at 150 U/ml; 2 h of incubation were required to reach the optimal response level. These stimuli can also induce IFN-gamma-pretreated neutrophils to release reactive oxygen species (ROS), such as superoxide anion, hydrogen peroxide and hypochlorous acid, as well as granule lysosomal enzymes and the pro-inflammatory cytokines TNF-alpha and IL-6. We found that increased expression of Fc gamma R, dectin-1 and complement receptors (CRs) correlated with these effects in these cells. The enhancing effect of IFN-gamma on the respiratory burst was found to be associated with up-regulation of the gp91(phox) and p47(phox) subunits of NADPH oxidase, as measured by their mRNA levels. The enhancing effect of IFN-gamma on phagocytosis and ROS release may not only be relevant for the efficient killing of invading microorganisms, but may also produce oxidative stress on adjacent cells, resulting in a possible inflammatory role that could also be favored by the liberation of the pro-inflammatory cytokines TNF-alpha and IL-6. (C) 2013 Elsevier B.V. All rights reserved.