PDF(Pubmed)
Abstract：
Listeria monocytogenes (L.m) is efficiently controlled by several cells of the innate immunity, including the Mast Cell (MC). MC is activated by L.m inducing its degranulation, cytokine production and microbicidal mechanisms. TLR2 is required for the optimal control of L.m infection by different cells of the immune system. However, little is known about the MC receptors involved in recognizing this bacterium and whether these interactions mediate MC activation. In this study, we analyzed whether TLR2 is involved in mediating different MC activation responses during L.m infection. We found that despite MC were infected with L.m, they were able to clear the bacterial load. In addition, MC degranulated and produced ROS, TNF-α, IL-1β, IL-6, IL-13 and MCP-1 in response to bacterial infection. Interestingly, L.m induced the activation of signaling proteins: ERK, p38 and NF-κB. When TLR2 was blocked, L.m endocytosis, bactericidal activity, ROS production and mast cell degranulation were not affected. Interestingly, only IL-6 and IL-13 production were affected when TLR2 was inhibited in response to L.m infection. Furthermore, p38 activation depended on TLR2, but not ERK or NF-κB activation. These results indicate that TLR2 mediates only some MC activation pathways during L.m infection, mainly those related to IL-6 and IL-13 production.
摘要：
单核细胞增生李斯特菌（L.M)由先天免疫的几个细胞有效控制，包括肥大细胞（MC）。MC通过L.m诱导其脱颗粒而被激活，细胞因子的产生和杀微生物机制。TLR2是免疫系统不同细胞对L.m感染的最佳控制所必需的。然而,对识别这种细菌的MC受体以及这些相互作用是否介导MC激活知之甚少。在这项研究中,我们分析了在L.m感染期间TLR2是否参与介导不同的MC激活反应.我们发现尽管MC感染了L.M,他们能够清除细菌负荷。此外,MC脱粒并产生ROS，TNF-α,IL-1β,IL-6、IL-13和MCP-1响应细菌感染。有趣的是,L.m诱导信号蛋白的激活：ERK，p38和NF-κB。当TLR2被阻断时，L.m内吞作用，杀菌活性，ROS产生和肥大细胞脱颗粒不受影响。有趣的是,当TLR2对L.m感染的反应被抑制时，只有IL-6和IL-13的产生受到影响。此外，p38激活依赖于TLR2,但不依赖于ERK或NF-κB激活。这些结果表明，TLR2在L.m感染期间仅介导一些MC激活途径，主要与IL-6和IL-13产生有关。
