动物造模 z-bio 2023-09-12 817

　　1. Toll like receptor 2 gene knockout mice. In Toll like receptor 2 gene knockout mice, homozygotes can survive and their appearance and behavior are normal. Macrophages from mouse bone marrow cannot trigger an immune response to the lipoproteins of Borrelia burgdorferi, but can be activated by non lipoproteins degraded by ultrasound. Compared with the control group, infection with Borrelia burgdorferi caused more severe arthritis in mutant mice. Compared to the wild-type mice in the same litter, the infected tissues of mutant mice can contain 100 times or even more bacteria. After infection, a high number of spirochetes can last for 8 weeks. When treated with LPS of Leptospira nephrosa, mutant homozygous mice neither produced TNF- α It cannot produce IL6 and will not develop disease.

　　2. Homozygotes of Toll like receptor 3 gene knockout mice can reproduce and survive with normal appearance and behavior. Mice produce splicing of a non functional gene product. Stimulation with Poly (I: C) polymyocytidine (a dsRNA synthetic analogue) resulted in the inability of mouse macrophages to produce the inflammatory cytokine IFN- γ And IFN- β。 Mice develop resistance to Poly (I: C) induced tremor and reduce IL-12 production levels. The spleen cells of mice cannot react with viral dsRNA and the production of IL-6 is reduced.

　　C3H/HeJ C3H/HeJ mice carrying spontaneous mutations in the Tlr4 gene are widely used in research on tumors, immunity, inflammation, sensory neurology, and cardiovascular biology. As a spontaneously mutated gene, Tlr4 lps provides its endotoxin resistance in the Toll like receptor gene of the C3H/HeJ mouse strain background. As a result, mice are highly sensitive to Gram negative bacterial infections, such as Salmonella. After infection with Salmonella, C3H/HeJ mice showed delayed production of chemokines, damage to NO production, and weakened cellular immune response. Infected mice die with an increase in bacterial growth within the liver Kupffer cell network.