Abstract
Background:Francisella tularensis, a causative agent of human tularemia, displaying the ability to proliferate inside the human cells. Aims: To evaluate the growth potential ofF. tularensisLVS strain in macrophage-like cell line J774 modulated by recombinant interferon γ andE. coliderived lipopolysaccharide. Results: Stimulation of J774 cells either by interferon-γ or lipopolysaccharide alone, or especially in combination before infectionF. tularensis, revealed protective effects. Higher concentrations of stimulating agents were needed to inhibit ongoingF. tularensisinfection. Conclusions: Stimulation of J774 cell line by combination of interferon-γ with lipopolysaccharide inhibits the intracellular growth ofF. tularensis.
Highlights
Francisella tularensis is a Gram-negative facultative intracellular bacterium and the causative agent of tularemia [12, 14], a severe and often fatal disease of human and other mammals [5]
We examined the abilities of the recombinant murine lymphokine INF-γ and/or LPS derived from E. coli to stimulate in vitro antimicrobial activity of macrophage-like J774 cell line against the live vaccine strain (LVS) of Francisella tularensis through the abilities of activated macrophages to reduce proliferation of this bacteria
Macrophage-like J774 cells were treated with 100 or 1000 IU/ml of INF-γ and/or 10 or 50 ng/ml of LPS that was added into infected cell cultures at the time 0
Summary
Francisella tularensis is a Gram-negative facultative intracellular bacterium and the causative agent of tularemia [12, 14], a severe and often fatal disease of human and other mammals [5]. Because of the practical and regulatory complications of work with fully virulent clinical isolates, most of the available studies of an early host response to F. tularensis have used the live vaccine strain (LVS), which is attenuated for humans but causes a fatal infection in mice [2]. Growth inside macrophages is a strategy that many prokaryotic and eukaryotic pathogens use to evade the host immune responses. Growth inside macrophages protects microbes during the acute phase of disease and serves as niche for the long-term survival of pathogens [6]. Biogenesis of the Francisellacontaining phagosome (FCP) is arrested for 2–4 hrs at a unique stage within endosomal-lysosomal degradation pathway, followed by gradual bacteria escape into cytosol, where the microbes are proliferating
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