Connell H, Hedlund M, Agace W, Svanborg C
Department of Medical Microbiology (Section for Clinical Immunology), Lund University, Sweden.
Adv Dent Res. 1997 Apr;11(1):50-8. doi: 10.1177/08959374970110011701.
Microbial attachment to mucosal surfaces is a first step in mucosal infection. Specific interactions between microbial surface ligands and host receptors influence the distribution of microbes in their sites of infection. Adhesion has often been regarded as a sufficient end point, explaining tissue tropism and bacterial persistence at mucosal sites. Adherence, however, is also a virulence factor through which microbes gain access to host tissues, upset the integrity of the mucosal barrier, and cause disease. The induction of mucosal inflammation is one aspect of this process. Bacterial attachment to mucosal surfaces activates the production of pro-inflammatory cytokines that cause both local and systemic inflammation. Epithelial cells are one source of these cytokines. The binding of fimbrial lectins to epithelial cell receptors triggers transmembrane signaling events that upregulate cytokine-specific mRNA and increase cytokine secretion. P fimbriae that bind the globoseries of glycolipids cause the release of ceramides and activation of the ceramide signaling pathway which contributes to the IL-6 response. Spread of cytokines and other pro-inflammatory mediators from the local site contributes to the symptoms and signs of infection.
微生物附着于黏膜表面是黏膜感染的第一步。微生物表面配体与宿主受体之间的特异性相互作用影响微生物在感染部位的分布。黏附通常被视为一个充分的终点,用以解释组织嗜性和细菌在黏膜部位的持续存在。然而,黏附也是一种毒力因子,微生物通过它进入宿主组织,破坏黏膜屏障的完整性并引发疾病。黏膜炎症的诱导是这一过程的一个方面。细菌附着于黏膜表面会激活促炎细胞因子的产生,从而导致局部和全身炎症。上皮细胞是这些细胞因子的一个来源。菌毛凝集素与上皮细胞受体的结合触发跨膜信号转导事件,上调细胞因子特异性mRNA并增加细胞因子分泌。与糖脂球系列结合的P菌毛会导致神经酰胺的释放和神经酰胺信号通路的激活,这有助于IL-6反应。细胞因子和其他促炎介质从局部部位扩散会导致感染的症状和体征。