

Acta Veterinaria et Zootechnica Sinica ›› 2025, Vol. 56 ›› Issue (10): 4863-4876.doi: 10.11843/j.issn.0366-6964.2025.10.009
• Review • Previous Articles Next Articles
WANG Hengtai(
), JIANG Hui, LI Peng*(
), DING Jiabo*(
)
Received:2025-01-10
Online:2025-10-23
Published:2025-11-01
Contact:
LI Peng, DING Jiabo
E-mail:17861509833@163.com;lipeng01@caas.cn;dingjiabo@caas.cn
CLC Number:
WANG Hengtai, JIANG Hui, LI Peng, DING Jiabo. Biosynthesis of Brucella Lipopolysaccharides and Their Biological Functions in Immune Evasion[J]. Acta Veterinaria et Zootechnica Sinica, 2025, 56(10): 4863-4876.
Table 1
Comparison of homology between Brucella lipid A-related synthesis proteins and other gram-negative bacteria %"
| 蛋白 Protein | 与铜绿假单胞菌相似性 Similarity with Pseudomonas | 与沙门菌相似性 Similarity with Salmonella |
| LpxA | 38.43 | 39.22 |
| LpxC | 43.11 | 39.22 |
| LpxD | 38.30 | 37.74 |
| LpxB | 32.44 | 32.58 |
| LpxK | 36.49 | 34.81 |
| LpxL | 36.49 | 34.81 |
Fig. 1
Schematic diagram of the hypothetical biosynthesis process of Brucella LPS M6P. Mannose-6-phosphate; M1P.Mannose-1-phosphate; GDP-M. Guanosine diphosphate-mannose; GDP-G. Guanosine diphosphate-glucose; GDP-4-keto-6-dMan. Guanosine diphosphate-4-keto-6-deoxy-D-mannose; GDP-4-amino-4, 6-dMan. Guanosine diphosphate-4-amino-4, 6-dideoxy-D-mannose; GDP-Perosamine. Guanosine diphosphate-4-amino-4, 6-dideoxy-D-mannose"
Fig. 2
The mechanism diagram of LPS in the immune evasion process of Brucella(S type) ①The long acyl chains of Brucella S-type LPS lipid A inhibit the recognition and binding of host TLR4/MD-2;②The low levels of phosphorylation and glycosylation of the core oligosaccharide of Brucella S-type LPS inhibit the binding of complement C1q;③The O-antigen of Brucella S-type LPS can bind to the scavenger receptor SR-A on host cell membranes, preventing early fusion with lysosomes, thereby ensuring the early survival of Brucella inside the cells; ④The O-antigen can spatially hinder the presentation process of MHC-Ⅱ, reducing the efficiency of antigen presentation; ⑤The O-antigen limits the activation of the NF-κB signaling pathway, promoting the survival of Brucella within cells; ⑥The O-antigen inhibits the formation of C3 convertase, reducing the production of pro-inflammatory cytokines and decreasing complement-mediated lysis, which facilitates Brucella survival within cells; ⑦The O-antigen suppresses the ER-Stress signaling pathway, benefiting Brucella's survival inside the cells; ⑧The O-antigen activates the PI3K/Akt signaling pathway in macrophages, promoting the survival of infected cells, which further enhances Brucella survival within cells. Here, C3a + C5a refers to the active peptides produced during the complement activation process—complement C3a and C5a fragments. PI3K/Akt refers to the phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt) pathway, which is crucial for regulating cellular processes such as growth, metabolism, and survival. ER-Stress describes a state where the endoplasmic reticulum function is disrupted or damaged. As a response mechanism, cells initiate adaptive processes to restore ER homeostasis, ensuring proper protein folding and normal cellular function. NF-κB refers to a family of transcription factors involved in immune responses, inflammation, cell proliferation, survival, and stress reactions"
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