通过降低氧化的稳定性,Calpain-2促进了细胞内细菌Listeria monocytogenes的感染和侵入肠道免疫屏障
Bo Yao1, Jingru Wang2, Dingyu Hou2
1College of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China; Department of General Practice, The Fifth Affiliated Hospital of Southern Medical University, Guangzhou 510900, China.
Journal of advanced research
|August 30, 2025
概括
卡尔帕因-2 (CAPN2) 通过破坏肠道免疫屏障中的氧化 (NO) 稳定性来促进Listeria monocytogenes的入侵. 向CAPN2可以预防细胞内细菌感染.
科学领域:
- 免疫学
- 微生物学
- 生物化学
背景情况:
- 卡尔派因 (CAPN1和CAPN2) 是参与各种生理和病理过程的酶.
- CAPN2在调节细胞内细菌感染和入侵方面发挥作用,但其机制尚未完全理解.
研究的目的:
- 研究肠道CAPN2在Listeria monocytogenes (L. monocytogenes) 感染中的作用
- 阐明L. monocytogenes通过皮耶尔补丁通过损害氧化 (NO) 稳态来侵入肠道免疫屏障的机制.
主要方法:
- 在小鼠中的L. monocytogenes感染模型,包括缺乏calpastatin (CAST) 或使用CAPN2抑制剂 (CAPN2-Inh) 的小鼠.
- 使用诱导性氧化合成酶 (iNOS) 淘汰小鼠对L. monocytogenes入侵,CAPN2激活和NO依赖性的研究.
- 使用流细胞计和光追踪分析NO的产生,L. monocytogenes的感染和细胞间传播.
主要成果:
- 在L. monocytogenes感染期间,CAPN2的激活和表达是动态的.
- CAPN2 调节 iNOS 介导的 NO 生产,从而影响 NO 稳定性,并促进 L. monocytogenes 侵入肠道免疫屏障.
- 抑制CAPN2或降低NO信号减少了L.单细胞体的增殖和细胞间的扩散.
结论:
- 通过依赖NO的机制,CAPN2的激活促进了L. monocytogenes的侵入.
- 针对CAPN2具有预防L. monocytogenes等细胞内细菌感染的治疗潜力.
相关概念视频
Nitric Oxide Signaling Pathway
5.2K
Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
5.2K
Caspases
12.7K
Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
12.7K
Gastritis-II: Pathophysiology
542
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
542
NF-κB-dependent Signaling Pathway
7.8K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
NF-κB-dependent Signaling Mechanism
The...
7.8K
Ligand-Gated Ion Channel Receptor: Gating Mechanism
2.6K
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
2.6K
Nociception
29.4K
Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain.
29.4K


