Host interferon-γ inducible protein contributes to Brucella survival.

Brucella spp. are highly adapted intracellular pathogens of mammals that cause chronic infections while surving and replicating in host monocytes and macrophages. Although monocytes are normally susceptible to infection, pretreatment with pro-inflammatory cytokine interferon-γ (IFN-γ) activates cellular defense mechanisms that increase intracellular killing of Brucella and prevents bacterial replication.

Large-scale purification of latex bead phagosomes from mouse macrophage cell lines and subsequent preparation for high-throughput quantitative proteomics.

Phagocytosis involves the engagement of a diverse array of cell surface receptors whose signal must be integrated on the membrane of the forming phagosomal cup. This method enables the quantitative proteomic analysis of phagosome fractions derived from phagocytes stimulated under two different conditions, thus allowing the complexity of phagosomal signaling to be analyzed in terms of the quantitative changes in phagosomal fraction protein content.

Induction of guanylate binding protein 5 by gamma interferon increases susceptibility to Salmonella enterica serovar Typhimurium-induced pyroptosis in RAW 264.7 cells.

The regulation of caspase-1 activation in macrophages plays a central role in host defense against bacterial pathogens. The activation of caspase-1 by the detection of bacterial products through Nod-like receptors leads to the secretion of mature interleukin-1beta (IL-1beta) and IL-18 and the induction of rapid host cell death (pyroptosis). Here, we report that pyroptosis induced by Salmonella enterica serovar Typhimurium can be positively regulated by prior gamma interferon (IFN-gamma) stimulation of RAW 264.