Abstract
To date, a variety of Brucella effector proteins have been found to mediate host cell secretion, autophagy, inflammation, and other signal pathways, but nuclear effector proteins have not yet been reported. We identified the first Brucella nucleomodulin, BspJ, and we screened out the BspJ interaction host proteins NME/NM23 nucleoside diphosphate kinase 2 (NME2) and creatine kinase B (CKB) through yeast two-hybrid and co-immunoprecipitation assays. These proteins are related to the host cell energy synthesis, metabolism, and apoptosis pathways. Brucella nucleomodulin BspJ will decrease the expression level of NME2 and CKB. In addition, BspJ gene deletion strains promoted the apoptosis of macrophages and reduced the intracellular survival of Brucella in host cells. In short, we found nucleomodulin BspJ may directly or indirectly regulate host cell apoptosis through the interaction with NME2 and CKB by mediating energy metabolism pathways in response to the intracellular circulation of Brucella infection, but the mechanism needs further study.
Highlights
Brucella infects animals and human beings and causes Brucellosis (Atluri et al, 2011), a major zoonotic disease endemic in more than 170 countries and regions of the world (Avilacalderon et al, 2013)
After pDsRed2-C1-BspJ was transferred into HEK293T cells, DAPI staining of the nucleus and scanning with a confocal microscope revealed that the BspJ protein was mainly located in the host cell nucleus, while it was not found in the control pDsRed2-C1 (Empty) (Figure 1A), which initially confirming our conjecture
The interactions between the proteins and BspJ were verified by CO-IP. After both of pcDNA3.1MIF/NME2/creatine kinase B (CKB)/ribosomal protein L13 (RPL13) and pcDNA3.1-BspJ was transferred into HEK293T cells, whole cell lysate (WCL) western blot analysis detected the presence of four proteins
Summary
Brucella infects animals and human beings and causes Brucellosis (Atluri et al, 2011), a major zoonotic disease endemic in more than 170 countries and regions of the world (Avilacalderon et al, 2013). Brucella’s survival, proliferation and parasitism depend on its Brucella abortus Nucleomodulin BspJ Targets Host Transduction intracellular circulation (including in macrophages and dendritic cells) in the host (Atluri et al, 2011; Celli, 2015). With Brucella proliferates in large numbers in rBCVs, it forms a recombinant rBCV called an autophagy BCV (aBCV) that releases mature Brucella to complete its intracellular circulation process and infect new cells (Celli, 2019)
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