Svanborg C, Godaly G, Hedlund M
Department of Microbiology, Immunology and Glycobiology Institute of Laboratory Medicine Lund University 223 Lund Sweden.
Curr Opin Microbiol. 1999 Feb;2(1):99-105. doi: 10.1016/s1369-5274(99)80017-4.
Mucosal pathogens use diverse and highly specific molecular mechanisms to activate mucosal inflammation. It may even be argued that their virulence depends on the inflammatory response that they induce. Some bacteria target epithelial cells and trigger them to produce inflammatory mediators but others cross the mucosa and activate macrophages or dendritic cells. Although systemic release of inflammatory mediators causes many symptoms and signs of infection, local chemokine production leads to the recruitment of inflammatory cells and lymphocytes that participate directly in the clearance of bacteria from mucosal sites. In this way, mucosal inflammation is a two-edged sword responsible for disease associated tissue destruction and crucial for the antimicrobial defence. Understanding of these pathways should create tools to enhance the defence and interfere with disease.
黏膜病原体利用多样且高度特异的分子机制来激活黏膜炎症。甚至可以说,它们的毒力取决于所诱导的炎症反应。一些细菌靶向上皮细胞并触发其产生炎症介质,但其他细菌则穿过黏膜并激活巨噬细胞或树突状细胞。尽管炎症介质的全身释放会引发感染的许多症状和体征,但局部趋化因子的产生会导致炎症细胞和淋巴细胞的募集,这些细胞直接参与从黏膜部位清除细菌。通过这种方式,黏膜炎症是一把双刃剑,既会导致与疾病相关的组织破坏,又对抗菌防御至关重要。对这些途径的了解应能创造出增强防御和干预疾病的工具。