Nucleomodulin BspJ as an effector promotes the colonization of Brucella abortus in the host

• Published in: Journal of veterinary science (Suwŏn-si, Korea) Vol. 23; no. 1; p. e8
• Main Authors: Ma, Zhongchen, Yu, Shuifa, Cheng, Kejian, Miao, Yuhe, Xu, Yimei, Hu, Ruirui, Zheng, Wei, Yi, Jihai, Zhang, Huan, Li, Ruirui, Li, Zhiqiang, Wang, Yong, Chen, Chuangfu
• Format: Journal Article
• Language: English
• Published: Korea (South) The Korean Society of Veterinary Science 01.01.2022; 대한수의학회
• Subjects: Animals; Brucella abortus - pathogenicity; Brucellosis - veterinary; Host-Pathogen Interactions; Interleukins; Mice; Original; Type IV Secretion Systems - genetics; 수의학; intracellular survival; clinical pathology; cytokines; Brucella abortus; secreted protein
• ISSN: 1229-845X; 1976-555X
• DOI: 10.4142/jvs.21224

infection induces brucellosis, a zoonotic disease. The intracellular circulation process and virulence of mainly depend on its type IV secretion system (T4SS) expressing secretory effectors. Secreted protein BspJ is a nucleomodulin of that invades the host cell nucleus. BspJ mediates host energy synthesis and apoptosis through interaction with proteins. However, the mechanism of BspJ as it affects the intracellular survival of remains to be clarified. To verify the functions of nucleomodulin BspJ in 's intracellular infection cycles. Constructed BspJ gene deletion strain ( ΔBspJ) and complement strain ( pBspJ) and studied their roles in the proliferation of both and . BspJ gene deletion reduced the survival and intracellular proliferation of at the replicating -containing vacuoles (rBCV) stage. Compared with the parent strain, the colonization ability of the bacteria in mice was significantly reduced, causing less inflammatory infiltration and pathological damage. We also found that the knockout of BspJ altered the secretion of cytokines (interleukin [IL]-6, IL-1β, IL-10, tumor necrosis factor-α, interferon-γ) in host cells and in mice to affect the intracellular survival of . BspJ is extremely important for the circulatory proliferation of in the host, and it may be involved in a previously unknown mechanism of 's intracellular survival.